molecular genetic evidence for a multipurpose genome

dear mammuthus,You say (among other things) in response to Fred's mail:FW:
Mammuth claims:1) Cheetah has the same amount of genetic information as its pre-bottleneck parent species. He can use the definition at the beginning of my post to make his case. If he cannot make his case with this definition, he can then attempt to use the even more watered-down definition, Shannon information, to make his case.
2) Monkenstick’s graph was somehow a good one, that it has something to say about whether or not non-random mutations exist.M: Let's actually look at what I said in response to Peter Borger post 57 as opposed to whatever Fred Williams wishes to attribute to me.PB:
CONSERVATION BIOLOGIST’S CONCERN ABOUT DWINDLING POPULATIONS IS BASED ON INBREEDING AND A DECLINE OF THE GENEPOOL. THIS HAS BEEN OBSERVED ON THE CHEETAH, THE FLORIDA COOGAR, ALLOCASUARINA, ETCETERA. IN MY OPINION, THE CURRENTLY LIVING ORGANISMS HAVE POOR GENOMIC CONTENT DUE TO LOSS OF GENETIC INFORMATION FROM THE MULTIPURPOSE GENOME.MY RESPONSE:
Maybe I should have said POORER genomic content. It is well established that distinct subpopulations of species have lost/diminished expression of different genes. In humans ADH, hemoglobin, CF are lost in distinct subpopulations, while other still have them. The redundant alpha-actinin 3 gene is lost in approx 18% in caucasion population without any survival effect.M: Then your assertion is falsified. They have niether poor genetic content nor have they lost genetic information. They have reduced allelic variation in the population i.e. cheetah's almost monomorphic. Since they are not extinct their genetic content is not poor.MY RESPONSE:
Maybe I should have said poorer compared to before the bottleneck. I really have to spell out everything I say, because you like to be deliberately obtuse. Furthermore you assert that they didn't loose genes. How do you know? Did you count genes before and after the bottleneck? And what also wonders me is your assertion that reduced allelic variation is the culprit. How do you know? You assume it. The observation of monomorphic genes is not equivalent to a decreased fitness. It doesn't matter for structural and metabolic proteins. It probably only matters for the immunological compartment. However, the immunological system generates its own mutations so over a few generations this system will be variable again. In addition, projects like HUGO show that we are not able to give the exact amount of genes of the human genome, indicating the high within species variability. Variability not through gain of new genes, rather through random loss of preexisting genes. These genes are apparently not directly necessary for survival/reproduction and will get lost easily. All in accord with the multipurpose genome.
Furthermore, your example of the cheetah also demonstrates that organisms have an excess of genes (redundancies) that can be lost. Still the organism survives: Redundancies of the multipurpose genome.M:
If you become extinct you sucked. If the genome is so multipurpose how can it have poor genetic content?MY RESPONSE:
The multipurpose gene is subject to entropy. Redundant genes will get lost easily. In particular those genes not immediately required for survival and reproduction.M:
Or are you saying that all individuals carry every bit of genetic variation within the population? If so this is easily falsified as well.MY RESPONSE:
Going back in time subspecies become more and more one species. This origin-species has got the ultimate genetic variation because it still contains all preexisting genes. Through genetic losses, and differential regulation of these preexisting genes it can adapt to a range of environments. For instance the Darwin Finches on isolated Galapagos isles. Cross breeding (as has been carried out) will increase the genetic variability through inbreeding of lost genes (distinct species lost different genes). Thus, the more variability is inbred the closer the organism will resemble the original 'kind' containing all original genetic info. Whether the original kind can ever be backcrossed remains to be established. My guess is NOT, since regulatory elements like retroviruses may have an irreversible effect on gene expression. So, in my opinion, the original genome is plastic within preset limits.M:
So I questioned if Peter Borger considers all INDIVIDUAL genomes to host the variation within the population i.e. multipurpose Lamarkian adaptation. Why is it a cheetah (individual)has a "poorer" genetic content now than prior to the bottlneck? They have the SAME genes, they are diploid, the sexually reproduce, etc etc like there ancestors. However, the cheetah population as a whole has less variation. That is the consequence of a genetic bottleneck....if they do not go extinct, they do not have "poor" genetic content. They have lost alleles not genes.MY RESPONSE:
Alleles of what? Regulatory networks? Immunogenes? Genes coding metabolism proteins? It all depends on the alleles you are referring to. Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are bot mutant alleles. Your explanation does not account for wild type alleles. You also have to consider the fact that monomorphic alleles (homozygous) genes is the rule rather than the exception in any organism studied. So, in my opinion, monomorphic genes cannot be the culprit. Loss of genes can be.M:
That Fred somehow connects the above argument with some fantasy about isolating poodles to produce St. Bernards is his own problem.MY RESPONSE:
No, it is an evolutionary problem. It cannot be explained by NDT, or the gain of new genes. It can be explained by the multipurpose genome: differntial loss and differential regulation of preexisting genes.M:
2) Monkenstick demonstrated random mutation i.e. provided evidence for it. That is more than you have done for non-random mutation. So it is a good one.Unless you will now magically produce the evidence for non-random mutation?MY RESPONSE:
Non-random mutaions have been demonstrated but every time evolutionist provide fallacies to overcome them. This is also clear from the Cairns excerpt in letter #52 in the "mol gen evidence against random mutaion thread" (Dr Page response to Fred). Let's have a look at this paper again and I will demonstrate where the evolutionist's reasoning goes wrong. I don't understand that it is not seen through by the molecular biologists involved.best wishes,
Peter[This message has been edited by peter borger, 11-05-2002]

Dear Mammuthus,Return to Start (mail #1). Read what the multipupose genome holds, than throw again.More soon.Best wishes,
Peter

Dear mammuthus,Your socalled 'bumped postings' are on Quetzal's selfinvented thread called "creatons and morphogenetic fields". Although it has been dedicated to me --I'm flattered-- we were discussing the multipurpose genome in the evolution section. The creaton-morphogenetics should be discussed in the origin of life/genes thread. Let's first continue the multipurpose genome debate. Next, we can discuss creatons in more detail. Thanks for your understanding and cooperation,Best wishes,
Peter

Dear mammuthus,Thanks for your response.You write:PB:
Maybe I should have said POORER genomic content. It is well established that distinct subpopulations of species have lost/diminished expression of different genes. In humans ADH, hemoglobin, CF are lost in distinct subpopulations, while other still have them. The redundant alpha-actinin 3 gene is lost in approx 18% in caucasion population without any survival effect.M: Can you give an example of diminished expression?MY RESPONSE:
LDH and ADH in asian populations.M:
Or do you just mean lost?MY RESPONSE:
Both diminished expression and lost genes is possible.M:
However, none of this is obvious from the cheetah. There is no evidence that they lost a gene like alpha actinin 3. And again, they are not extinct so their "quality" is fine.MY RESPONSE:
Non-scientific humbug. A fine quality of cheetahs? And what about the fine quality of the Allocasuarina? Also of fine quality? In a previous letter it was stated that they struggle to survive, characterised by degenerate sperm production, high newborns deathrates, etc. It demonstrates loss of genes, not monomorphism of genes.
In addition, I predict that even this empoverished genepool of the cheetah will still have genetic redundancies.PB:
Maybe I should have said poorer compared to before the bottleneck. I really have to spell out everything I say, because you like to be deliberately obtuse.M: You have a knack for vaguery that makes it impossible to always know what you are talking about. "poor" genomic content is a meaningless statement.MY RESPONSE:
Talking about vaguery. According to Quetzal evolutinism predicts either statics or dynamics. That's not even vague, that's nothing! It predicts nothing!!! Compared to wild types, poor genetic contents are often observed in laboratory animals. Did you know that laboratory mice can vary in genomic content between 3-3.3 billion nucleotides per diploid genome? That is 10%.PB:
Furthermore you assert that they didn't loose genes. How do you know? Did you count genes before and after the bottleneck? And what also wonders me is your assertion that reduced allelic variation is the culprit. How do you know? You assume it. The observation of monomorphic genes is not equivalent to a decreased fitness.M: I guess you did not read any of the papers.MY RESPONSE:
I do not see a link between my statements and your answer. Clearly, your conclusions are base upon assumptions. That's not science, that's wishful thinking.PB: It doesn't matter for structural and metabolic proteins.M: Do you know this or are you just saying this?MY RESPONSE:
Obtuse again? It is known from elementary biological knowledge, and you also (should) know that's better to have the wild type than the mutant form for such genes.PB:
It probably only matters for the immunological compartment. However, the immunological system generates its own mutations so over a few generations this system will be variable again. In addition, projects like HUGO show that we are not able to give the exact amount of genes of the human genome, indicating the high within species variability.M: Why would we know a priori the exact number of genes? HUGO used extremely rough calculations and were wrong...and?MY RESPONSE:
Are you going to say that all human subpopulation have the same genetic content (same amount of genes)? If so, you are wrong (as demonstrated in previous mails distinct subpopulation will loose distinct genes, since it is a random process). This has been sceintifically proven beyond any doubt.PB: Variability not through gain of new genes, rather through random loss of preexisting genes. These genes are apparently not directly necessary for survival/reproduction and will get lost easily. All in accord with the multipurpose genome.M: How do you know if the genes are new or not with the multipurpose genome?MY RESPONSE:
New protein families. Although you probably doubt them, they are for sure around. For instance recombination proteins (RAG1 and RAG2)in mammals that are involved in gene rearrangemnt in B cells to optimise antigen-antibody interactions. They are found only in mammals with such adaptive immune systems, and they are new genes present in the multipurpose genome of mammals.M:
Since you claim that no animals are similar due to common descent you therefore don't know if New World Monkeys developed before or after humans by your hypothesis.MY RESPONSE:
This question cannot be addressed by science (similar to the origin of gene, as discussed before). It can also not be addressed by evolutionism. It can only be speculated upon and the answer depends on the paradigms one proposes.M:
All genes could be new or old. They could have been created as the sequencing reaction occurred to give the appeareance of the appearance of common descent. How you going to test for that. I have also given you citations for novel genes in primates but you choose to ignore them. And do you really claim ALL variability you see is due to loss of genes?.....Hartl and Clark...Hartl and ClarkMY RESPONSE:
Novel genes is primates doesn't make it easier for evolutionists. Now you have to explain them. Duplication and random mutaion would be my guess. If so, let's discuss the redundant alpha actinin genes. It immediately falsifies this vision.PB:
Furthermore, your example of the cheetah also demonstrates that organisms have an excess of genes (redundancies) that can be lost. Still the organism survives: Redundancies of the multipurpose genome.M: You still don't understand the concept of fitness do you?MY RESPONSE:
Again, you do not respond to my statements. You are starting to behave like Dr Page. He's got a degree in elusiveness.PB:
The multipurpose gene is subject to entropy. Redundant genes will get lost easily. In particular those genes not immediately required for survival and reproduction.M: Then it is pretty freaking amazing that so many redundant genes are highly conserved....or now you are going to post the exact same above sentence but just put a "not" in fron of subject in the first sentence?MY RESPONSE:
Back to start, Mammuthus. You didn't read or didn't understand, what I wrote in mail #1. If you reread it you will notice that stability of DNA sequences is secured by DNA stabilising and repair proteins. That's a prediction of the hypothesis of multipurpose genome and it has been demonstrated to be correct in even the simplest organisms studied.
Why would I post exactly the same sentence? I know what I am talking about and I can explain all biological phenomena with the hypothesis of the MG.MY RESPONSE:
Going back in time subspecies become more and more one species. This origin-species has got the ultimate genetic variation because it still contains all preexisting genes.M: I actually asked if you think each (not the species) individual genome contains the variation of the species? That would fit with Lamarkian dynamics.MY RESPONSE:
No, I already said --and this is observed in populations-- that losses are at random. So, the genepool of all populations of (sub)species contain what is left over of the original multipurpose genome. It is easy to understand (sub)speciation from this stance. Remember Occam's rasor? The easier the solution the better.PB:
Through genetic losses, and differential regulation of these preexisting genes it can adapt to a range of environments. For instance the Darwin Finches on isolated Galapagos isles. Cross breeding (as has been carried out) will increase the genetic variability through inbreeding of lost genes (distinct species lost different genes).M: You forgot that selection acts on the random mutation in the Darwin finches with those best adapted to the new environment surviving and reproducing.MY RESPONSE:
Selection is not in doubt here. Random mutation is in doubt here. Studies on birds beaks demonstrate that all the variation is already within the gene pool, selection of certain characteristics of the beak can be selected against. For instance, drought will give birds with small beaks a disadvantage due to hard seeds. They will be selected against, and these genes may be removed from the gene pool if drought persists. So, here we have a nice example of reduction of genetic content. The opposite is also possible. However, the loss of such gene can be restored in the population by breeding.M:
The birds don't just fly out one day and there beaks morph....and please explain how cross breeding will increase genetic variability through inbreeding since cross breeding and inbreeding are opposites.MY RESPONSE:
Slip of the pen. It should have read cross breeding, not inbreeding.
Cross breeding will restore genetic variability. In addition, you have to explain the beak in the first place. I mean an evolutionary explanation for the genetic program that gave rise to the first beak.M:
Hybrids are usually less fit than either parent species and populations of such hybrids usually die out unless the two species share a hybrid zone...look it up.MY RESPONSE:
What hybrids? You mean a hybrid between sheep and goat, for instance.
So, please be specific and look it up.PB:
Thus, the more variability is inbred the closer the organism will resemble the original 'kind' containing all original genetic info.M:Inbreeding reduces variability. More inbred individuals do not look like the last common ancestor or do you think the Amish are more genetically similar to Homo erectus because they are more inbred than the average human population?MY RESPONSE:
Here I also meant crossbreeding.M:
Also you seem to imply that the first breeding pair of a species contains all genetic variation possible for that species and must reproduce through some alternative means to suddenly make a population appear that contains all the variation which is then subsequently lost..disregarding expanding populations for one thing...and you think evolutionary theory is in trouble???MY RESPONSE:
I already explained how the multipurpose genome works. Preexisting DNA elements induce variability due to differential regulation, and is probably partially irreversibel due to the character of these elements. I guess you would call these elements retroviroids, or LINE's or SINE's. Or whatever you call them.PB:
Whether the original kind can ever be backcrossed remains to be established. My guess is NOT, since regulatory elements like retroviruses may have an irreversible effect on gene expression. So, in my opinion, the original genome is plastic within preset limits.M: To bad this is not a testable hypothesis...preset by whom?MY RESPONSE:
As if evolutionism is a testable hypothesis. It has been tested and falsifies over and over.
Preset by the multipurpose genome, of course. The Creator if you like.PB:
Alleles of what? Regulatory networks? Immunogenes? Genes coding metabolism proteins? It all depends on the alleles you are referring to. Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are bot mutant alleles.M: Hmmmm have you ever studied genetics? Are you really really sure that "Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are bot mutant alleles"? Ever hear of dominant mutants? Partial dominance? Penetrance? Genetics 101 Peter.MY RESPONSE:
Yep, any idea about the mechanisms underlying dominant mutations, and penetrance?PB:
Your explanation does not account for wild type alleles. You also have to consider the fact that monomorphic alleles (homozygous) genes is the rule rather than the exception in any organism studied. So, in my opinion, monomorphic genes cannot be the culprit. Loss of genes can be.M: Funny then that for many genes heterozygosity is very high.MY RESPONSE:
That point in the direction of non-random mecahnisms. All in accord with the multipurpose genome.M:
In fact it is variable among species with those going through bottlenecks showing very little like W. nobilis to those with very high relative heterozygosity.MY RESPONSE:
The Wollemi pine doesn't demonstrate very little, it demonstrates NO variation. Wanna play the same game as Quetzal, with his distortion of scientific observations?PB:
No, it is an evolutionary problem. It cannot be explained by NDT, or the gain of new genes. It can be explained by the multipurpose genome: differntial loss and differential regulation of preexisting genes.M: Okay, then you finally have a testable hypothesis. You can isolate a group of poodles like Fred says and you should get St. Bernards if you agree with his prediction..this is not a predicition of evolutionary theory but obviously one of multipurpose-ism.MY RESPONSE:
No, it is YOUR prediction and based upon lack of understanding of the hypothesis of the MG. The actual prediction made by the MG is that due to lost genetic sensible-sequences --not due to genetic monomorphism as you may think-- it is impossible to get St Bernards, or backcross a wolflike animal. However, if you artificially select certain dogs you will be able to generate a wolflike animal from the complete gene pool of the subspecies of dogs. Thus, you bring together all genes that are still present in the gene pool in one organism. Next, you can start breeding with this 'restored multipurpose genome' and you can get the St Bernard, the poodle, the dachshund, the chihuahua, etc.PB:
Non-random mutations have been demonstrated but every time evolutionist provide fallacies to overcome them.M: If by demonstrating you are wrong is how you define fallacy then so be it. Monkenstick at least provided a graph..let's see yours.MY RESPONSE:
I commented on his graph. What I meant is the comments of evolutionists in response to the adaptive mutations of Raddman (mail#52 mol. gen. ev. against random mut. thread). It demonstrates that evolutionists overbluff Raddman (a molecular biologist) by their assertions that "..the error prone polymerase has been selected for their ability to allow cell to cope with damage; the generation of variability [in the genome due to this error prone polymerase] may simply a non-selected byproduct". Well, dear evolutionists, do you really understand biology? I have the feeling that they don't, since it makes the polymerase redundant and since they are not under selective constraint evolutionism predicts highly variable DNA sequences with respect to redundant gene. Based on the MG, I predict that knocking out the errorprone polymerase doesn't effect the organism at all. So here you have another problem.
Contrary what evolutionists believe and propagate as fact, molecular biology is not in accord with evolutionism.PB:
This is also clear from the Cairns excerpt in letter #52 in the "mol gen evidence against random mutaion thread" (Dr Page response to Fred). Let's have a look at this paper again and I will demonstrate where the evolutionist's reasoning goes wrong. I don't understand that it is not seen through by the molecular biologists involved.M: Let's have a look at some of my and Quetzal's unanswered questions to while we are at it.MY RESPONSE:
As mentioned before, I will answer (and rebut) all your questions. Easy, since evolutionism is false.Best wishes,
Peter[This message has been edited by peter borger, 11-06-2002]

Dear Dr Page,You write:quote:
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Originally posted by peter borger:
Dear Dr page,
Your definition was oldfashioned (as expected, since evolutionism is an outdated theory). If you include introns in your definition, you also have to include all regulatory elements: promoters, enhancers, silencers etc. Enhancers and silencers have been found 10-100 thousand bp up- and down-stream of the coding sequences of a gene.So, here we have the upgraded 21st century definition of a gene: All sensible-sequences that contribute to regulated expression of another sensible-sequence (specifying either protein or RNA).Maybe you didn't get it yet, but biology is moving fast.best wishes,
Peter--------------------------------------------------------------------------------Hey look! It is Fred Williams long-lost love child!MY RESPONSE:
New for me.You:
But tell us all, Pete, what that has to do with referring to an exon as a gene?I:
Ask dr Kim.You:
And do you have a soure for your definition?I:
It is elementary that genes are regulated by distant DNA elements. That you didn't know that is because it is not your field, I guess.You:
You see, maybe you just don't know better-- you are an asthma researhcer-- so you can be forgiven}...I:
Best wishes,
peter[This message has been edited by peter borger, 11-06-2002]

Dear Quetzal,Quote:
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I've had a good look at figures of Dilwynite- and Wollemia pollen and it is easy to discriminate between the two. So, this argument fails. Show me the figures where they demonstrate that the pollens of dylwinites and wollemia pollen are indistinguishable.
--------------------------------------------------------------------------------Q: I gave you the reference, look it up for goodness sake!PB: I’ve seen a full colour photograph of dylwinites and wollemia’s pollen and even a blind person can see the difference. Present the figures here you refer too. Or send me a copy (Dr P. Borger Uni of Sydney). If you are right I will admit it, but you are wrong, I’ve seen the pollens. I can send you a copy, if you wish.quote:
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Probably so, or probably not? Of course this the evolutionary vision and I am aware of it. It does however NOT explain the invariability in the region that are usually highly variable regions. That was my point and still is my point. It tells me that DNA sequences are stable throughout time and that difference between individual trees is not likely to be due to pointmutations, but rather through differential gene regulation. Differential regulation probably involves the histon code.
--------------------------------------------------------------------------------Q: So, anything written by an evolutionary biologist, botanist, geneticist, etc is by definition incorrect according to your view? Continue to believe whatever you wish. You’ve been shown to be wrong — repeatedly.PB: Mantra’s. Dr Page’s club?Q: I have cited multiple references, and every single article ever published on Wollemia nobilis. If you wish to continue arguing that the authors of these studies are completely wrong, there’s not much I can do to convince you otherwise.PB: Listen Quetzal, I take time to provide you with an alternative vision, so at least you could give me the impression that you actually try to respond to that. Otherwise, be silent, and I don’t waste my time. For the last time, the authors demonstrate NO variability and even for me as a non-native English speaker that is something completely different than LOW variability. Even to an evolutionist this should be obvious.quote:
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Demonstrate where the data are erroneous and incomplete, back it up with refernces.
--------------------------------------------------------------------------------Suggest you actually go back and read all the references I’ve provided. Your interpretations have been shown to be erroneous. The data is incomplete because Peakall hasn’t completed the study — the initial sequencing was done on only 18s (by Peakall), and rcbl by (Setaguchi et al), references for which you have already been provided. This means that your assertion that this flipping tree somehow proves multipurpose genomes are absolutely stable and evolutionary theory completely overthrown is based at best on limited data from an initial study.MY RESPONSE:
These data are the only data published in peer reviewed scientific journals, you mean. All sequences analysed thus far were found to be invariable between the different stands. So, my claim stands as long not proven otherwise.
You also like to exaggerate. The tree violates molecular evolutionism, so evolutionism cannot be true, and thus cannot be presented as fact. That’s what you want to do, present it as scientific fact, while it isn’t. The tree brings further doubt upon evolutionism. You know that. You simply ignore it, like you do with all evidence against evolutionism. You’re a faithful believer.quote:
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Of course I am not being taken seriously by evolutionists. When I registered to this site it was one of the first things that came into my mind as a possible evolutionist's fallacy: O this guy doesn't understand anything about biology, so we don't have to take him seriously. I am used to that fallacy already.
--------------------------------------------------------------------------------Q: If I didn’t think you were serious, I’d have ignored you completely. However, you have shown your ignorance or willful misunderstanding of even basic biology every time you type a new response.PB: The usual response. I don’t understand this and I don’t understand that. I can assure you that I as a molecular biologist specialised in eukaryotic gene regulation I much better understand evolutionism and the underlying mechanism than Dr Page (he is anatomist by education) or you (a conservationist). So, it is you who doesn’t understand the molecular mechanism involved in evolutionism. So, don’t even try it. I know it is a common fallacy of evolutionists. Either this fallacy or complete silence. Evolutionism is NOT in accord with molecular biology.quote:
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Furthermore, I don't know exactly how you make up your mind but I have the feeling that as long as an evolutionary vision hasn't been put forward, you simply do not know what to say about the data. For the rest you adapt to any evolutionary explanation that comes by, without objectively looking at the plausibility of the explanation. In contrast, I can immediately recognise whether molecular data are in accord with evolutionism or not. And I don't buy far-fetched evolutionary explanations anymore, since I can make up stories myself.
--------------------------------------------------------------------------------Q: Yet another personal attack. Nope, wrong again. Since I’m not the one actually performing the original research, I tend to listen to the folks that are.PB: Nope, you do NOT listen to molecular biologists who say that evolutionism is not in accord with current understanding of contemporary biology. Everyone can see this now. You do not accept any of my mails of being relevant against evolutionism. You only listen to evolutionary explanations. You cannot think beyond that outdated paradigm. Don’t play the innocent, Quetzal, since it won’t work. I can see right through your biased responses.Q: When what they are saying contradicts other things — either my own personal observations or some other scientist — I dig into the subject in more depth and make up my own mind. On the other hand, I tend to only reference articles in these discussions which I agree with — otherwise I wouldn’t post them. Not my fault if the articles contradict your little fantasies. And I agree — you’re great at making up far-fetched stories.PB: If so, than you also know that the Wollemia violates molecular evolutionary rules. Even Dr. Peakall acknowledged it.quote:
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Finally, the case of Wollemia is extreme AND unusual. Even Dr. Peakall acknowledged that. If it is so common, give me the references please that show NO variability in subpopulations of organisms.
--------------------------------------------------------------------------------Q: I did — I referenced several plants, a couple of mammals, etc. Pay attention. If you can’t keep up, take notes.PB: No you didn’t. These references demonstrate LOW variability. You are distorting the scientific content. NO doesn’t equal LOW.quote:
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All your answers are biased by the axioma "evolution is true". You are unable to think beyond this axioma. Probably --most likely-- the axioma you live with is wrong, and I provided a different explanation, that may be wrong but --most likely-- it may as well be right.
--------------------------------------------------------------------------------Q: Whether it’s true or not is what we’re discussing, isn’t it? So far, you’ve shown a grand total of zip, zilch, nada that indicates you’ve falsified evolution as you’ve claimed. You haven’t even raised a decent question yet. The only thing you’ve done is make unsupported assertions and refused to answer direct questions.PB: And the denial continues. Welcome to Dr Page’s club (I guess Mammuthus is a member too, now). Listen, Quetzal, one cannot discuss with people who deny scientific observations. It clearly demonstrates that evolutionism isn’t science; it’s just another -ism. If you demonstrate that the trees are variable in the expected regions I will be the first to admit it, since I am a scientist, and I don’t deny observations.Q: Tell you what: here’s my axiom (and so you’ll stop claiming I don’t know anything). For me, to understand biodiversity and the birth and death of populations and species — and how to preserve them - requires an understanding of the natural history and ecology of individual species, and the biology of the individual organisms that make up the species. Survival of populations in the wild is dependent on effective population size, distribution, and density. The number of birds crammed into a small forest fragment or the number of algae cells on a wet rock effects food supply, how heavily predators and pathogens strike, to what degree reproduction is delayed or effective, how long individuals live, which new competitors can force themselves into the community, etc. To understand life, you must specify the context — the parameters of which are a function of a particular time and place. To understand biodiversity, you have to understand the processes of speciation and extinction - the birth rate of new species and the longevity of the clades they in turn spawn. You have to understand the first order effects of any environmental change, and the second-order ripples they cause, the third-order changes caused by the second, etc. And you need to understand the natural history underpinnings of the creation of ecosystems — because no organism on the planet lives in isolation. That is where my axiom comes from. Creaton waves, magical multipurpose genomes, spurious non-random mutations do absolutely NOTHING to advance my understanding of the processes that are critical to my work. Every single plant, animal, insect or fungus that I’ve ever encountered; every single interaction in the wild I’ve ever studied, merely confirms what science tells me about evolution. Hope that answers your question Dr. Borger.PB: And what does all this have to do with an axioma? Let alone with the axioma of evolutionism? Nothing at all.
Regarding your professional interests, I don’t understand your objections to a multipurpose genome, since it also explains these phenomena, including the Wollemi pine. You say: To understand biodiversity, you have to understand the processes of speciation and extinction - the birth rate of new species and the longevity of the clades they in turn spawn. As long as you hang it on an evolutionary framework, you will never understand the underlying mechanisms. It is impossible to draw sound conclusions from a false theory. My advice: have a look at the raw data and analyse them without bias. That’s the way that leads to objective truth.quote:
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I could tell Dr Peakall about my vision, but I guess that I will have similar responses as I get from you, mammuthus, Dr Page. So, why bother. His assertion of an all-purpose genome was in response to the invariability between the two stands. Now there are even three stands. This is the context of his 'all-purpose genome': "Whatever crash-tackled the tree, one of the most conservative organisms that life has ever thrown up, must have been bordering on apocalypse. So seriously", Peakall told me, "the best genetic constitution hasn't been able to get it out of the canyon. But the flipside is, once it settled down in there its all-purpose genome has allowed it to do as well as it can. I think there's a lot of luck in this story." (The wollemi pine, J. Woodford in discussion with Dr Paekall. Page 171) So, Dr Peakall acknowledges --actually invents-- an ALL-PURPOSE genome.
--------------------------------------------------------------------------------Q: I’m still waiting for you to contact him for an explanation. If you think he’s so dead certain about the reality of your assertion, you should be jumping at the chance.PB: I didn’t know you were waiting. I will send him an email (do you still have his address?).quote:
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You didn't provide an explanation. Even Dr Paekall didn't have an explanantion. Why? Because there is NO evolutionary explanation. You are free to think that you have provided an explanation, but I know better from a molecular stance.
--------------------------------------------------------------------------------{Begin Borger mode}You’re just so wrapped up in your dogmatic assertion of creatons and multipurpose genomes that you can’t accept any other explanation.{/Borger mode} I’ve given you several explanations from pop gen and ecology that could account for the limited variation in this species. Try actually developing a logical argument against them — like tell me WHY clonality, or extreme bottleneck, or any of the other explanations don’t make sense. All you’re doing is handwaving — in fact, if you hand wave much more you’re going to achieve liftoff.PB: Indeed. You (and a lot of other evolutionists) have been so brainwashed that you (they) are unable to think beyond the paradigm of evolutionism. I know your explanations. They do not make sense in the light of molecular evolutionary rules. I explained that several times. You don't listen.quote:
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All mainstreams explanation you provided end in a dead alley. I wouldn't have had a problem with the Wollemia nobilis if there was only one stand with identical DNA. Now there are two (or three) identical populations that cannot have been cloned from each other, I --and with me Dr Peakall-- have a severe molecular evolutionary problem with the tree. I pointed this out in my previous letter, but you just don't seem to get my --and Dr Peakall's-- point.
--------------------------------------------------------------------------------Q: Okay, so I stand corrected: you HAVE received a response from Dr. Peakall. Please post it so we can all see how much he supports your position.PB: Being deliberately obtuse is another evolutionist’s fallacy, I’ve discovered on this site. I referred to an interview with Dr Peakall in Woodford’s book, as mentioned. I recommend you to buy a copy of this interesting book.quote:
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Your idea is that small populations are highly susceptible to diseases since they are gentcally uniform. Maybe your idea is wrong. Judging the Wollemia the are perfectly able to survive under several different conditions. Even in the city of Sydney I've encountered them. So, that is the multipurpose genome in action. Furthermore, I wonder whether you can provide evidence for your assumption that genetically uniform populations are more prone to diseases or that this observation merely reflects loss of genetic information that leads to extinction upon unusual stimuli from the environment (diseases). I guess this is a chicken-egg problem, so my vision against yours.
--------------------------------------------------------------------------------Q: Even in the city of Sidney you’ve encountered them? Amazing — and here I’d thought everyone was saying they were rare. Oh, you mean you encountered them in the controlled environment of a botanical garden or institute? Bit of a different story, that.PB: No, they are not in a controlled environment and are free to contact with all possible pathogens imaginable (where do you get your info? Mine is first hand, I've seen them). None of the trees demised. Sounds a lot like the multipurpose genome to me.Q: There’s quite a bit in the literature on disease and bottlenecks — my suggestion would be to read some conservation biology. Look up feline infectious peritonitis and check out the FIP outbreak in African cheetahs in East Africa during the 1980’s. There was also a mini-epidemic at the Los Angeles Zoo. In every other species that can be infected by this virus, the mortality rate is about 1%. The 1980’s outbreak in cheetahs was 60% fatal. Do some actual research for a change before you claim that the scientists studying an issue are wrong.PB: Thanks. Could you make a link to these references? In addition, why didn’t all cheetahs die? Any idea?quote:
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(I read somewhere that the current population of the oryx was bred from 2 individuals and the alleged extinct cape lion has been found in a Russian zoo and all descended from a couple left there by a circus in the previous century. The concept of inbreeding and enhanced susceptibility to diseases doesn't seem to account for these organisms, including Wollemia. It is a questionable concept.)
--------------------------------------------------------------------------------Q: Of course you have references for your oryx assertion, right? I mean which species are you talking about: O. gazella, O. tao, O. beisa, O. leucoryx? Your extremely sloppy scholarship is showing again - you are once more making utterly spurious assertions about what scientists are doing with absolutely no effort on your part to either learn about or understand what it is you’re attacking.PB: I was hoping you could bring some light in what I read. And, you being obtuse again, I didn’t bring it as scientific fact. So, please shine some light on this matter.
It is always fun to kick butt on a tangent, isn’t it? Characteristics of Dr Page’s club.Q: As to the cape lion — what’s your point? Two cubs were imported to South Africa from Siberia — but they’re a related subspecies. There are, however, 11 reported specimens of what may be descendants of the cape lion in Ethiopia. Even if they are — and aren’t hybrids with another lion subspecies - as far as I know no genetic tests have been performed (except to show the Siberian cubs were a separate subspecies). So asserting that they are or are not genetically homogenous is pretty speculative, even for you.PB: They were pretty viable, weren’t they? No bottleneck phenomena?Q: Of course you’re correct that there’s no risk of pathogens with Wollemia either. That’s undoubtedly why they’ve instituted a complete contamination barrier — including forcing the scientists studying the trees to wash their boots in antiseptic before working with the wild populations — because they’re unconcerned about the introduction of new pathogens.PB: All according to current evolutionary paradigm, that (very) probably isn’t right. The multi-purpose genome makes it less likely that the Wollemi pine will immediately be killed by pathogens. Now, the pine is growing everywhere —not only in restricted areas-- , is able to encounter loads of potential pathogens, and nothing happened. So, the MPG is far superior here.quote:
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My response: endstations can indeed go extinct. Either endstations stay unchanged for eons or they go extinct. Could & Eldredge wrote extensively on this observation.
--------------------------------------------------------------------------------Q: No, you misunderstood — endstation as I used it IS extinction. Otherwise the population continues to evolve. When it can’t, it goes extinct. Gould and Eldredge wrote extensively on the mode and tempo of evolution, they didn’t talk at all about endstations or whatever. Now Vrba wrote quite a bit about extinction and selection sweep. Maybe you’re confused.PB: Here you demonstrate that you are unable to think beyond the evolutionary paradigm. All organism we have ever observed or present in the fossil record are endstations and will eventually become extinct. There is no evolutionary mechanism that can bring them to another level, since it requires reprogramming if the genome.
[It can only be performed by fast (there possibly are also slow) creatons. ]quote:
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Q: As to your comment on breeding, you are again in error. In fact, one of the main management concerns with relict populations is finding ways to preserve the existing genome of the organisms. For example, the Catalina mahogany consists of six adult trees in two karyotypes (of which one is a known hybrid). To prevent further hybridization, one recommendation I saw was to cut down the hybrid! Another example is another Australian relict, Haloragodendron lucasii, which consists of a total of 8 populations but only 7 genetic individuals. In fact, one population (of some 700 specimens), contained only 3 different genetically distinct individuals! Isolation, small population size, inbreeding depression, clonality, etc ALL contribute to homogeneity in genomes in once widely variant populations. Beyond that, speciation has nothing to do with 'loss of information' whatever that means.PB: I presume that the individuals of these organism demonstrate genetic differences? So, there is no threat to evolutionism. Why bother about hybrids, it merely demonstrates that they are of the same kind. If these organism are able to form hybrids with other organisms what is the problem? Does the hybrid have more or less distinctive genes? Does the genepool increase by cutting the hybrid down?Loss of information has nothing to do with speciation? Get familiar with contemporary biology is my advise.--------------------------------------------------------------------------------Q: Read what I wrote! It’s quite straight forward conservation biology. 700 specimens, all genetically related to only three individual genotypes in a single population. And yes, there are genetic differences — don’t tell me you don’t know what a karyotype is I’ll leave you to guess why your questions on the debate over the Catalina mahogany hybrid show you don’t have the first clue what you’re talking about.PB: I know what a karyotype is. However, it doesn’t contribute to an increased gene pool. I was interested in the sensible-sequences in the subpopulations. Is there a difference with respect to order of genes and/or nucleotides? That would be far more interesting. And why do you leave me to guess? I am genuinely interested in this matter. So, please expand.quote:
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PB: Please provide the reference for the lizard. I will check it on DNA analysis. I expect not to find the change at the nucleotide level (as for the bacteria), but rather on the level of gene expression. This has also been demonstrated in mice. For instance, the agouti-colour is non-mendelian inherited. It depends on a jumping DNA element (usually referred to as a retroviral element) that affect the expression of the agouti-gene.
--------------------------------------------------------------------------------Q: I did give you the complete reference. (Hint: look at the original post. See the little line under the title? Click on it and you have access to the original article in the original journal). What the hell does color inheritance in mice have to do with population bottlenecks or even conservation of isolated populations? Nice attempt to baffle with bs by dragging in a complete irrelevancy in an apparent attempt to show off how much you knowPB: Thanks for the reference. I will check it out.
That you don’t understand or miss to see the link doesn’t make it irrelevant.quote:
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Q: Evolution predicts both variation and stasis, depending on the particular organism and the environmental factors that effect it.
PB: Of course. I could have expected this. In other words evolutionism doesn't predict anything. Pretty bad for a theory.
--------------------------------------------------------------------------------Q: Now you’re back to denying organisms have a natural history. Oh yeah, I forgot — magical creaton waves poofed them into existence de novo.PB: Strawman attack. Natural evolutionary history or natural multipurpose history? That’s the question.quote:
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Yes, and evolutionism doesn't predict anything. I will work on the inconsistencies if they are present. However, the rule on this planet is that species suddenly appear, do not change over time and then become extinct. Pretty much in accord with my hypothesis and not in accord with the gradual changes required by evolutionism.
--------------------------------------------------------------------------------Q: I assume this is the Peter Borger Rule of Biodiversity? Again, depends on the organism in question, the environmental factors impinging on it, etc. Some lineages change — speciate — quite readily, others don’t. There’s a lot of interesting debate over the causal factors of this difference.PB: A lot od uninteresting evolutionary oldfashioned outdated humbug you mean? Some lineages change others don’t sound like directed evolutionism (did you read davison’s papers). All in accord with the hypothesis of a multipurpose genome.quote:
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Sensible-regions are regions that have a function and do therefore not change. These regions make sense, therefor sensible region. They can be protein coding regions, but also regions that code RNAs involved in regulatory mechanism, regions involved in lining up chromosomes during cell divisions, etcetera. More and more RNA consensus sequences are discovered that are required for gene expression. It will be a major part of the 'junk-DNA'.
--------------------------------------------------------------------------------So sensible regions are exons? What happens when one of the various mutations occurs in these sensible regions?PB: Quetzal, there are a lot more sensible regions than exons. Even introns are sensible, spacers are sensible, promoters are, enhancers are, silencers are, all tRNA gene are, all regulatory RNA genes are, masking sequences are, and every day we discover more sensible-sequences involved in gene regulation. Here you demonstrate that you are not up to date with contemporary molecular biology. For a recent definition of a gene ask Dr Page, I mailed it to him, very recently. Usually, mutations are detrimental for the sensible-sequences. I well established observation in biology.quote:
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No, Dr Borger agrees with Dr Peakall that evolution is not sitting well here. He says: 'Wollemia is likely the exception that disproves the rule. The assumption has been made that genetic variability is good because it is the basis of natural selection. The Wollemi pine might actually proof that in some systems it is possible to have exceptionally low variability and stay reasonable happy' (page 170). In my opinion, the Wollemi pine is not an exception but the tree is the extreme of the multipurpose genome. It is proof for a multipurpose genome.
--------------------------------------------------------------------------------Q: I’d like you to post the response from Dr. Peakall where he says evolution isn’t sitting well — not the Woodford quotation — the response to your email that you’ve apparently received from him. I’ve never said — nor has any biologist that I’ve ever read — that low variability is a guarantee of extinction, although it's usually a good sign the population is in serious trouble.PB: It is an interview --for that matter a quotation-- in Woodford’s book. What’s your problem with his words? To me his words a pretty clear. It not greek or chinese, so how can it be so unclear to you?Q: I also agree that Wollemi Pine isn’t an exception — just an extreme example of a normal distribution. As far as variability is good, although a gross oversimplification, in essence this is true. It’s the key to your question above concerning disease susceptibility. I’m surprised I have to explain this basic concept. The more genetically homogenous a population, the less likely it will contain adaptive variants able to survive or take advantage of new selection pressures. IOW, introduce a new pathogen into a population with lots of variation, there’s much more likelihood that there will be some individuals in the population with at least partial resistance to the pathogen. In a homogenous population, the odds of having an individual or group with resistance is much less, and hence if a pathogen effects one individual, it will effect ALL the individuals in the population.PB: I also agree that the Wollemi pine is an extreme. Namely the extreme of the multipurpose genome. It is able to fight off pathogens due to the preexisting information in the MG.quote:
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Q: No, youre changing your statement. You said that the DNA was incapable of variation.
PB: No, I didn't say that. Reread my first mail, where I roughly outlined the concept of the multipurpose genome.Q: Since this is completely counter to all observations and published literature, I am more than justified in asking for evidence of YOUR claim. Show that there is a mechanism, structure, or chemical that prevents Wollemia (because that was the organism we were discussing) from varying.PB: Of course I do not have to prove an absence. The authors already showed that where variability was expected it wasn't found. In addition, I didn't say that DNA is incapable of change, but the mechanisms my be different than assumed. Change at the single nucleotide level is not a major change inducing mechanism. Rather, shuffling of DNA elements that affect gene expression will do the trick. All evidence currently present points in this direction. You may call that evolution, I know it isn't. It is variation induction through preexisting genetic elements. Probably the genome of Wollemia --and other members of the Araucariacaea-- still specifies the most optimal array of DNA repair enzymes.--------------------------------------------------------------------------------Q: Sorry Peter, your message 16 on this thread specifically states the DNA is unvariable, i.e., not capable of variation. You have been challenged to show the mechanism by which DNA is prevented from variation. Your assertion = your evidentiary support required. Try again.PB: Obtuse again? I asked to have a look at my first mailing, i.e. mailing #1 of this thread. Now you refer to message #16. Message #1 is able to cover all biological phenomena. Message #16 refers to sensible-sequences.quote:
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As demonstrated above, I will. Present the literature if you are so sure.
--------------------------------------------------------------------------------Q: I have. You have not produced ONE SINGLE PIECE OF EVIDENCE outside Woodford’s book. I have presented you with numerous articles from peer reviewed journals written by the scientists actually studying the issue. Your entire argument thus far rests on your continual restatement that they don’t know what they’re talking about.PB: Why would I retract an sound scientific observation? As long Peakall and colleugues don't demonstrate variability I will not retract? Give me at least a good reason why I would retract on the invaraibility of the trees?quote:
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Sometimes I wonder why do I still discuss with evolutionism-believers. They are so stuck in their own paradigm that they are unable to think otherwise. Even if it has been falsified over and over.
Free your mind and I will show you the world how it really is.--------------------------------------------------------------------------------Q: Thanks, I’ll decline. I get enough of a rush out of the real world — I don’t need to accept your fantasy.PB: Of course you don’t have to accept a new theory immediately. Over the long run, however, you will have since it better describes what we observe and that is what it is all about in science. Description of observations.quote:
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Dr Peakall was the first scientist I heard talking about an All-Purpose genome and he further opened my eyes. I think that Dr Peakall tries to get his data in accord with evolutionism since he has to 'publish or perish'. So he introduces things like the exception that proves a rule. With believers of evolutionism as the only peers for scientific journals he will have a pretty hard time to get it in if he didnt do that, dont you think so? The hypothesis of the multipurpose genome holds that stability ensuring DNA repair mechanisms (plus the redundant genetic code) keep the DNA sense-sequences from changing. The variation observed (since not all the tree are the same) is due to jumping/shuffling DNA elements that affect gene regulation.
Besides, you demonstrate that you don't understand my hypothesis. The hypothesis of MP is an alternative for evolutionism and often it is superior in explanations.--------------------------------------------------------------------------------Q: Please quote the response you received from Dr. Peakall. You’re spending a lot of words explaining to us ignorants here on this board what he really means. I challenged your interpretation using what Dr. Peakall actually wrote. Unless you can bring me Dr. Peakall’s exact response, then you are engaging in yet more baseless assertion.PB: Since you are questioning Peakall’s words, it is you who should contact Dr Peakall, not me. I don’t doubt his words.Q: Wait a sec, I just caught this — from the above, it now appears you are stating that there IS variation in the trees — which is what I’ve been saying for 9 pages. Have you retracted your assertion, and I missed it?PB: Yes, if you have a close look at a trees’s stand --for instance there are 10 in Taronga Zoo-- and it is clear that they are not identical. This has also been observed in cloned sheep. So there is a mechanism beyond DNA sequences that is able to induce change. I guess one of them is determined by the histon code.Q: As for not understanding your hypothesis — on the contrary, I at least understand what you’ve presented so far. I also understand that it’s completely spurious, based on utter lack of evidence and gross misunderstanding of basic conservation biology, genetics, ecology, etc. Misunderstandings which you repeatedly and effectively demonstrate all on your own every time you post. Keep it up — you’re making my argument better than I ever could.PB: You are definitively a member of Dr Page’s club. Denial and ignorance.
How can I discuss with guys who ignore scientific observations? Impossible.quote:
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What I mean is that all DNA elements required to phenotypic adaptations are already present in the multipurpose genome. For instance, the multipurpose genome has a program for sexual reproduction as well as a program for copicing. The environment simply demands which one (or both) is operative. If sexual reproduction hasn't been sensed for a while, this information is transmitted to the roots and the copicing program is initiated. Both programs can only be kept in the genome through preservation of the programs and that demand for an array of stability ensuring DNA replication mechanisms. It is an example of genetic redundancy and redundancies demand elaborate repair systems, otherwise they will be lost through entropy.
--------------------------------------------------------------------------------Q: I think Mammuthus already hit you on this one. However, so I understand you, are you saying that all organisms possess a multipurpose computer system that allows them to switch genetic programs at will?PB: Obtuse again. Mammuthus didn’t hit anything substantial, so far. Read what I said about these two reproductive systems and try to understand it. One is activated if the other isn’t sensed any more. Ever heard of inter- and intracellular signalling?Q: If every organism had a multipurpose genome — which is what you assert — every organism should be able to fill every niche on the planet at will. Great! I want to have a gill system that allows me to forego SCUBA gear. How do I turn on the ability to breathe water?PB: The MG is limited and not all organisms have the same to start with. The MG will become more and more limited over time due to losses and entropy. I mentioned this over and over. It is not a difficult concept to understand.quote:
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Q: Now we're getting somewhere. If I understand what you just wrote, any organism that can be shown to have developed any new (i.e., not transposed or whatever), completely novel gene will utterly destroy your theory? Please tell me that's the case, then we can stop these lengthy responses and all go do something useful.
PB: If you can unequivocally proof that this completely novel gene came about without the interference of creatons, it would be bad for the hypothesis. For instance, the TcR gene in mammals seem to drop out of the sky (O I see, the current story is 'birth-and-death-evolution and purifying selection'). What's wrong with the idea of creatons?. Nobody ever saw birth and death evolution, and nobody ever saw a creaton. So, there is no difference (except that evolutionism is scientifically accepted).--------------------------------------------------------------------------------Q: Great! Your hypothesis is falsified:PB: Even if it was (but it isn't), so what? The hypothesis of evolutionism has been so many times falsified that unbiased well informed biologists (NOT evolutionists) don’t even take it serious any more.QNurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL (1998), Selective sweep of a newly evolved sperm-specific gene in Drosophila, Nature 396:572-575quote:
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The pattern of genetic variation across the genome of Drosophila melanogaster is consistent with the occurrence of frequent 'selective sweeps', in which new favourable mutations become incorporated into the species so quickly that linked alleles can 'hitchhike' and also become fixed. Because of the hitchhiking of linked genes, it is generally difficult to identify the target of any putative selective sweep. Here, however, we identify a new gene in D. melanogaster that codes for a sperm-specific axonemal dynein subunit. The gene has a new testes-specific promoter derived from a protein-coding region in a gene encoding the cell-adhesion protein annexin X (AnnX), and it contains a new protein-coding exon derived from an intron in a gene encoding a cytoplasmic dynein intermediate chain (Cdic). The new transcription unit, designated Sdic (for sperm-specific dynein intermediate chain), has been duplicated about tenfold in a tandem array. Consistent with the selective sweep of this gene, the level of genetic polymorphism near Sdic is unusually low. The discovery of this gene supports other results that point to the rapid molecular evolution of male reproductive functions. (emphasis added)
--------------------------------------------------------------------------------Q: Here’s a brand new gene that was formed from bits and pieces of other genes — not a duplication event.PB: A brand new (?) gene from bits and pieces preexisting in the genome you mean? Sounds like a paradox. By shuffling I guess. As predicted by the multipurpose genome you mean?
And the selective sweep evo-non-sense. It is equivalent to Noah’s Ark. Very unscientific, and easy to falsify (as I demonstrate for the putative selective sweep to explain the non-variable human ZFX region).Q: Here’s the follow-up paper: Nurminsky D, Aguiar DD, Bustamante CD, Hartl DL (2001), Chromosomal effects of rapid gene evolution in Drosophila melanogaster, Science 291:128-130PB: I will look into it. Bet it is non-random evolutionism, parasite-host related, or an immuno-gene.quote:
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Rapid adaptive fixation of a new favorable mutation is expected to affect neighboring genes along the chromosome. Evolutionary theory predicts that the chromosomal region would show a reduced level of genetic variation and an excess of rare alleles. We have confirmed these predictions in a region of the X chromosome of Drosophila melanogaster that contains a newly evolved gene for a component of the sperm axoneme. In D. simulans, where the novel gene does not exist, the pattern of genetic variation is consistent with selection against recurrent deleterious mutations. These findings imply that the pattern of genetic variation along a chromosome may be useful for inferring its evolutionary history and for revealing regions in which recent adaptive fixations have taken place.
--------------------------------------------------------------------------------Q: Note the comparison with D. simulans, which has a recent —observed — common ancestor with D. melanogaster and DOESN’T have the gene.PB: Do you really understand these references, evolutionism and multipurpose genome? I don’t see a problem here. It is all in accord with a multipurpose genome and loss of genes, and selection against. Reread my mailing #1.Q: As to proving it didn’t happen through creatons — lol. You haven’t shown anything even remotely resembling proof that the silly things even exist! Why on Earth would you think I have to prove their absence in this process?PB: You’ve just found yourself another straw-man. You haven’t rebutted any of my claims anywhere in your mailings. All your references demonstrate is the multipurpose genome in action but discussed subject to the false paradigm of evolutionism. Get real, Q, nothing evolved here. It demonstrates the plasticity of the multipurpose genome and how variation is generated. I will spell out the papers and show you that my vision is as right —probably betterin explaining the data.quote:
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Q: I just had to include this section. I'm only going to cite one article out of hundreds that explains how ridiculous this assertion is, and how little you understand of population genetics, speciation, etc: Close genetic similarity between two sympatric species of tephritid fruit fly reproductively isolated by mating time.
PB: Please provide the reference you cite from. That these organisms seem to be speciating can be due to loss of DNA compatibility, so I don't see a problem for my hypothesis here. Also Darwin thought he saw speciation on the Galapagos Archipelago in all the different 'species' of finches. However, we now know that they can still interbreed and are thus NO new species. It is in favour of the plasticity of the multipurpose genome (that is due to loss of genes, and differential gene regulation due to shuffling DNA elements).--------------------------------------------------------------------------------Q: In the first place, I did provide the full reference (click on the title). Amazing you can make the assertion that the speciation event is due to loss of DNA compatibility whatever that is.PB: It needs a bit of an effort and a lot of free unbiased thinking to set up a new theory. All characteristics you seem to lack, judging from your mails.Q: How’d you arrive at that bit of inference when you haven’t, by your own admission, even read the article? From the title? Lol!!!! You didn’t even read THAT correctly. It talks about mating time incompatibility - one of several pre-zygotic barriers (in this case, behavioral, not genetic, originall). Your turn — provide a reference that shows the 13 species of finches on the Galapagos still interbreed.PB: Obtuse again? If your letter demonstrates anything here, it is the impossibility to discuss with brainwashed evolutionists. You’re almost Dr Page. I recommend you to read Nature and Science on the finches: the recent volumes not the volumes from Darwin’s age. Get updated with biological science, it would improve our discussion a lot.quote:
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The regions that are expected to change over time, and were expected to demonstrate variability, have been analysed and didn't show variability. Why would one analyse regions that are not expected to give a lot of change? Dr Peakall knows what regions to analyse in Araucaria family and he did just that. With the know results. Furthermore, coppicing could explain the invariability within the three stands NOT between the three stands.
--------------------------------------------------------------------------------Q: See above — way above.PB: Where, in the blue sky? Watch them fly? Quetzal, neither you nor anyone else solved the riddle around the Wollemi pine’s DNA (yet). You know that, but you prefer to be deliberately obtuse/in denial/ignoring. I am not impressed. Neither by your rebuttal, nor by your knowledge on contemporary biology.quote:
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Q: 1. With your extensive knowledge of population genetics, I'm sure you know that inbreeding depression and mutational load can counteract each other in very small populations. Although possibly an extreme example of this, the observation that Wollemia shows negligible variation at the loci thus far compared between stands could be related to this. In other words, there may not be significant change due to mutation because, if two of the stands were originally seeded from one tree (which hasn't been shown one way or the other), under even theoretically ideal conditions, the divergence would possibly be minimal over several generations.
PB: No, it is the extreme example of the multipurpose genome, characterised by stability of DNA sequences.--------------------------------------------------------------------------------Q: This is now the THIRD time you’ve failed to even address this issue beyond simply re-asserting your original claim. I can only assume that in spite of your vaunted, self-proclaimed expertise, you are unable to do so.PB: I will not repeat myself again. I recommend you to brush up on molecular biology and molecular evolution, so you can judge for yourself where evolutionism clashes with molecular biology.quote:
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Inbreeding depression and mutational load counteractions sounds interesting. Could you please provide a reference for this, since I am going to look into the genetics. I mean maybe an alternative genetic program has been switched on in this situation. Next, I will explain my vision on this topic.
--------------------------------------------------------------------------------Q: Tell me something Peter: are you simply incapable of looking something up on your own? This is pretty basic stuff. Here’s some articles I happened to have on my hard drive without even bothering to check Pubmed or any of the journals:Bataillon T, Kirkpatrick M (2000) Inbreeding depression due to mildly deleterious mutations in finite populations : size does matter! Genet. Res., 75 : 75-81Willis, JH (1999), Inbreeding Load, Average Dominance and the Mutation Rate for Mildly Deleterious Alleles in Mimulus guttatus Genetics 153: 1885-1898Colas B, Olivieri I, Riba M (1997) Centaurea corymbosa, a cliff-dwelling species tottering on the brink of extinction: A demographic and genetic study, PNAS 94: 3471-3476Reinartz JA, Les DH (1994) Bottleneck-induced dissolution of self-incompatibility and breeding system consequences in Aster furcatus (Asteraceae), Am. J. Bot. 81: 446-455Charlesworth D, Morgan MT, Charlesworth B (1992) The effect of linkage and population size on inbreeding depression due to mutational load Genet. Res., 59: 49-61PB: Immediately clear. Mildly deleterious mutations = loss of (redunant) genes. Why are you so blind? Are you paid to be so blind?Q: These should be enough to give you at least some education in the subject. Feel free to ask if you have any questions ONCE YOU’VE ACTUALLY READ THE ARTICLES. I’m getting really, really, REALLY tired of doing your research for you. For someone who throws their academic credentials at me every single chance he gets, you seem to be oddly incapable of looking up the basic concepts of the multiple scientific disciplines you claim to refute.PB: I will read the articles and demonstrate where they support the multipurpose genome.quote:
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A mutation not in the germ line and therefor not inherited by sexual reproduction. However, it can be expected that plants that rely on copicing will demonstrate somatic mutations --even in the 18sRNA or rcb genes. Why, since they tissue derived from rapidly dividing meristemes, and here mutations can be introduced easily. All sister cells grown from the mutated cell will also inherit the mutation. So, somatic mutations are expected. If not, the DNA is extremely stable, and in accord with the prediction done by the multipurpose genome.
--------------------------------------------------------------------------------Q: How about we see what the actual data says — WHEN IT’S FINALLY PUBLISHED.PB: Excellent idea. We will see what the data say. I don't need a data interpretation, I can do that myself. Unbiased. Keep me informed, since you seem to know Peakall.quote:
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Q: 4. All of your junk DNA, redundancies, etc, would only appear/accumulate in separated populations of multiple organisms over many generations. With Wollemia we are essentially dealing with three organisms only (although that may change with more data), not three populations. That's the implication of the coppicing growth pattern from an original seeding.
--------------------------------------------------------------------------------Q: You have once again failed to address this issue in any way whatsoever other than repeating your mantra. Try again.PB: Now you are starting to comment on your own replies? Confused? I have to repeat my statements since they are right. Your statements are wrong.quote:
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Q: No, we were talking about the tree. However, just to get rid of your horseshoe crab nonsense right from the start, the living members of this group consist of three distinct genera and five species.
PB: Show me the DNA analysis and the references. I have the feeling that you still don't understand what I am trying to convey. Speciation can readily be understood from a multipurpose genome, it doesn't need evolutionism.--------------------------------------------------------------------------------Q: No — you made the claim. You show ME the references that indicate the five species of horseshoe crab are genetically identical in accordance with your multipurpose genome.PB: Quetzal, I did a prediction from the MG hypothesis. So, now I like to see the refernces about the genera and subspecies so I can check it. That's how science works. So, could you please provide me with these papers. I would be grateful.Q: Your MG thingy is incredibly elastic, depending on what you’re responding to:PB: That's the good part about the MG hypothesis. It can explain every biological phenomenon (sounds like evolutionism, isn't it?).Q:
1. MG is indicated by invariant DNA (Wollemia) which prevents speciation.
2. MG is indicated by the existence of different species which have invariant DNA ()
3. MG can cause speciation, which, according to you, doesn’t exist.
4. Under the MG, genomic plasticity (in invariant DNA?) is due to loss of genes (but I thought it was invariant?).You aren’t even consistent in what you claim for your spurious hypothetical genome.PB: Excellent. You demonstrate here that you are able to rewrite MY hypothesis and than bring it down. How do we call that? Distortion, red herrings and Strawman attacks? CONGRATULATIONS!!!! You managed to introduce three fallacies in one response. (Nice try, try again)
In the meantime the MG still stands and is superior to eolutionism since it can explain ALL biological phenomena. Evolutionism can not.quote:
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Q: That enough variation for you? 'Living fossil'' 'lol' another 'argument from journalistic sensationalism'. Peddle it to someone who doesn't know any better. As to the designation of organism in the case of Wollemia, pending further data, I'd have to say each stand likely represents a single organism (or close enough as no matter).
PB: Even if they were, the separated populations are expected to demonstrate variability. You keep denying that. Maybe you should talk to Dr Peakall about it, since you don't want to accept it from me.--------------------------------------------------------------------------------Q: The point is, if the stands DO represent only three individuals — rather than three populations — seeded from a single individual, almost no variation would be expected. And you’re right about one thing, I wouldn’t accept uncorroborated ANYTHING from you at this point. Go ahead and contact Dr. Peakall for his input. I might accept what he has to say about the organism he’s studying.PB: I quoted Peakall already for you. What do you want? Peakall’s life act on a videotape?Best wishes
Peter

Dear QuetzalA couple of weeks ago I promised to demonstrate a species with NO genetic variability and not a clone. I did that. You deny that. I don't mind, it is the usual evolutinist's tactics.One final essential question --the quintessence-- for you:Do the --in a peer reviewed sceintific journal published (i.e. your refernces)-- genetic data on the Wollemi pine demonstrate LOW variability or do they demonstrate NO variability?Furthermore, if the overturn of evolutionism had to be based on this organism alone I wouldn't have even bothered to register to this site. It's just another death blow.Apparently you didn't read my posts. I am wasting my time here, that's for sure.And remember, there is a lot more in this world than evolutinism. You only have to open your eyes to see it. And I do not personally attack you, I attack evolutionism --this silly outdated hype that contradicts molecular biology-- and is propagated by a small group of atheists, calling themsleves scientists. Therefore I recommended you to read some books on the stuff, so you can judge for yourself. How these guys blind you, I mean, with their meaningless stories. Not to belittle you.Best wishes,Peter[This message has been edited by peter borger, 11-07-2002][This message has been edited by peter borger, 11-07-2002]

Dear mammuthus,
thanks for your response, here is my reply:M: Can you give an example of diminished expression?PB: LDH and ADH in asian populations.M: And the gene pools of Asians are poorer, better, equal to others based on this expression difference?PB: To my knowledge, no studies on this topic, yet. Considering the LDH and ADH genes, they are present in the gene pool but less expressed. A more obvious example is melanin in African and European population. The gene is present in both gene pools but differentially expressed.M: However, none of this is obvious from the cheetah. There is no evidence that they lost a gene like alpha actinin 3. And again, they are not extinct so their "quality" is fine.PB: Non-scientific humbug. A fine quality of cheetahs? And what about the fine quality of the Allocasuarina? Also of fine quality? In a previous letter it was stated that they struggle to survive, characterised by degenerate sperm production, high newborns deathrates, etc. It demonstrates loss of genes, not monomorphism of genes.
In addition, I predict that even this empoverished genepool of the cheetah will still have genetic redundancies.M: Lions which are not nearly as inbred as cheetah's also suffer from the above i.e. low sperm production etc. Which genes did the cheetah specifically lose...it should be obvious...you could try to PCR 18S rDNA and would not be there for example. Do cheetah's have more, less, equal numbers of ERVs as before? Are there chromosomes now shorter because of all this genetic loss you claim there is evidence for or do you mean genetic variation in the population? If you mean the latter it argues against multipurpose genome by the way.PB: 18S? Why 18S? It is an essential gene, so losing it will immediately be selected against. Why not tRNA genes? They are abundantly present, and can to a certain extent be lost.M: You have a knack for vaguery that makes it impossible to always know what you are talking about. "poor" genomic content is a meaningless statement.PB: Talking about vaguery. According to Quetzal evolutinism predicts either statics or dynamics. That's not even vague, that's nothing! It predicts nothing!!! Compared to wild types, poor genetic contents are often observed in laboratory animals. Did you know that laboratory mice can vary in genomic content between 3-3.3 billion nucleotides per diploid genome? That is 10%.M: 3.3 billion nucleotide variation in an inbred strain of mouse? Considering they have a genome similar in size to ours that is way more than 10% Peter. You sure you were looking at mouse and not C. elegans in your comparison? As to Quetzal being vague..he has given the conditions under which one expects sequences to remain static or to vary. That you ignore it is not his problem.PB: the genomic content of mice varies between 3 +/- 0.3 billion nucleotides per diploid genome.PB:
I do not see a link between my statements and your answer. Clearly, your conclusions are base upon assumptions. That's not science, that's wishful thinking.M: As I said you did not read the papers where this is discussed..or are you now claiming that all vets are full of shit to like every other biologist besides you?PB: Explain, I don’t get it.PB:
Obtuse again? It is known from elementary biological knowledge, and you also (should) know that's better to have the wild type than the mutant form for such genes.M: I'm obtuse? You might want to actually be sure your statement about mutant genes is truePB: It is elementary that the wild type gene is superior to a mutant gene in the genetic background of that gene. Denying that is denying biology.M: Why would we know a priori the exact number of genes? HUGO used extremely rough calculations and were wrong...and?PB: Are you going to say that all human subpopulation have the same genetic content (same amount of genes)? If so, you are wrong (as demonstrated in previous mails distinct subpopulation will loose distinct genes, since it is a random process). This has been sceintifically proven beyond any doubt.M: And will gain genes and will shuffle genes and will acquire mutations in genes. Show me the citation for the extreme change in number of genes in the human gene pool...I would love to see a new Hox gene in population XPB: Due to such mechanism the genetic content of seperated population will not be the same. Soon, the differences between human subpopulation will be elucidated. It is already known that different subpopulations lost distinct genes. I already mentioned the alpha actin gene: completely lost in 18% of the Caucasian population. The CFTR gene: 1 in 25 are carrier of the inactivated (=loss) gene in Caucasian population, etc. Easy to understand from MG stance.
I also would like to see a completely new gene in a human subpopulation.PB: New protein families. Although you probably doubt them, they are for sure around. For instance recombination proteins (RAG1 and RAG2) in mammals that are involved in gene rearrangemnt in B cells to optimise antigen-antibody interactions. They are found only in mammals with such adaptive immune systems, and they are new genes present in the multipurpose genome of mammals.M: How do you know they are new? Mammals by your definition only appear similar because non-random process. There is no reason for a mouse to be any more related to other mammals than to a liverwort. Or are you now backing away from your illusion of descent argument? You cannot on the one hand group mammals but then claim there is only identity by descent at the subspecies level.PB: Novel systems need novel genes and gene programs. The RAG2 doesn’t demonstrate homology with other known protein.PB: This question cannot be addressed by science (similar to the origin of gene, as discussed before). It can also not be addressed by evolutionism. It can only be speculated upon and the answer depends on the paradigms one proposes.M: That is if one just ignores the science on the subject. Considering that I, Quetzal, and others have to post links to the topics and ALWAYS find scientific citations for all of the points you claim are unknown, not thought about, or not studied your above claim is rather dubious and your scholarship is rather poor in this matter. I find that strange as you appear to be rather passionate about this subject yet refuse to inform yourself in any depth.PB: I can find these references myself. I can read them myself, and discover that all data are discussed subject to evolutionism. Next, I object to the just so stories presented by the authors, post my comments here, provide another solution to the data, usually an equal solution and often a better solution. What happens? You deny it, Quetzals denies it, Dr Page denies it, and he scoffs it. So, what is the use of reading these severely biased evo-stories. I know the content already. There is nothing new in it for science, no challenge, nothing! And nothing at all for mankind. Meaningless nothingness.MY RESPONSE:
Novel genes is primates doesn't make it easier for evolutionists. Now you have to explain them. Duplication and random mutaion would be my guess. If so, let's discuss the redundant alpha actinin genes. It immediately falsifies this vision.M: I have already provided a reference (more than once on this topic)...so go ahead..start the dicussion....PB: Refernce? Where can I find it, I will discuss it with you.M: You still don't understand the concept of fitness do you?PB: Again, you do not respond to my statements. You are starting to behave like Dr Page. He's got a degree in elusiveness.M: I don't respond? You have left almost all of my questions hanging without answers for weeks now so you are being rather hypocritical. I have explained this point to you before and get tired of repeating it. Do you understand what fitness is? From your answer I assume no, but I am getting sick of doing your homework for you.PB: If you mean the letters 94-96, I missed them, but will repond to them soon. Sick of doing my home work? If you wanna back up your assertions you have to do your homework. It is you who claims that all life we observe came about by pure coincidence and randomness, so you better provide me with compelling evidence, instead of the stuff usually provided by evo’s. As demonstrated these data can be explained according to the multipurpose genome equally well or better.PB: The multipurpose gene is subject to entropy. Redundant genes will get lost easily. In particular those genes not immediately required for survival and reproduction.M: Then it is pretty freaking amazing that so many redundant genes are highly conserved....or now you are going to post the exact same above sentence but just put a "not" in fron of subject in the first sentence?PB:
Back to start, Mammuthus. You didn't read or didn't understand, what I wrote in mail #1. If you reread it you will notice that stability of DNA sequences is secured by DNA stabilising and repair proteins. That's a prediction of the hypothesis of multipurpose genome and it has been demonstrated to be correct in even the simplest organisms studied.
Why would I post exactly the same sentence? I know what I am talking about and I can explain all biological phenomena with the hypothesis of the MG.M: Then you have failed to explain variation in the genes encoding the repair proteins, the variation in repair mechanisms, the extreme variation in repair fidelity among repair enzymes etc etc...which explains why DNA can vary as much as it does...hardly argues for your stabilizing by repair...in fact it falsifies it.PB: Ever heard of entropy? Differential regulation of gene expression due to Shuffling DNA elements? All provided by the MPG hypothesis. Yes, Mammuthus, it explains all biological observations.PB:
Going back in time subspecies become more and more one species. This origin-species has got the ultimate genetic variation because it still contains all preexisting genes.M: I actually asked if you think each (not the species) individual genome contains the variation of the species? That would fit with Lamarkian dynamics.PB: No, I already said --and this is observed in populations-- that losses are at random. So, the genepool of all populations of (sub)species contain what is left over of the original multipurpose genome. It is easy to understand (sub)speciation from this stance. Remember Occam's rasor? The easier the solution the better.M: Except that you would have to postulate that humans do not reproduce sexually and are not diploid since transfer of ALL variation from one generation to the next does not happen in a two sex diploid system...it does not work with any reproductive system known...hey, you do believe that storks bring babiesPB: Why would I have to postulate non-sexual reproduction of humans? Why would it be necessary to transfer ALL variation at once? It is merely your introduction of a straw man.M: You forgot that selection acts on the random mutation in the Darwin finches with those best adapted to the new environment surviving and reproducing.PB:
Selection is not in doubt here. Random mutation is in doubt here. Studies on birds beaks demonstrate that all the variation is already within the gene pool, selection of certain characteristics of the beak can be selected against. For instance, drought will give birds with small beaks a disadvantage due to hard seeds. They will be selected against, and these genes may be removed from the gene pool if drought persists. So, here we have a nice example of reduction of genetic content. The opposite is also possible. However, the loss of such gene can be restored in the population by breeding.M: Agree with most of this paragraph...wow,imagine that..except for the part about the variation always being there..I thought you said it gets lost by entropy..now you say it has to be maintained by cross species hybridization? Where is that stabilizing of the repair system? There should be no variation at all? Selection is not in doubt???PB::
Slip of the pen. It should have read cross breeding, not inbreeding.M: Fair enough.PB:
Cross breeding will restore genetic variability. In addition, you have to explain the beak in the first place. I mean an evolutionary explanation for the genetic program that gave rise to the first beak.M: Why do I have to explain the origin of the beak to explain beak evolution in Galapagos finches??? We can debate the subject if you wish but it is off the topic at hand.PB: If you want to discuss minor beak variations between subpopulations of finches, you first have to explain the beak, since the beak has an evolutionary origin too, according to your worldview. So, please explain. Other wise we simply discuss population genetics and that’s NO evolution. That is frequency changes of preexisting DNA elements over time.M:
Hybrids are usually less fit than either parent species and populations of such hybrids usually die out unless the two species share a hybrid zone...look it up.MY RESPONSE:
What hybrids? You mean a hybrid between sheep and goat, for instance.
So, please be specific and look it up.M: So yet again I have to do your freaking homework...you must be the laziest anti-science person I have ever met. Even Behe does his own background research....na ja.PB: No, you have to back up your extraordinary claim that all life evolved from nothing through randomness and selection. I will look up your references. Probablyy, the reduced fitness is related to an incompatible secondary DNA code, or maybe incompatible transcriptional code. Will read them. Thanks.M: Take your pick...Sage RD, Heyneman D, Lim KC, Wilson AC. Related Articles, LinksWormy mice in a hybrid zone.
Nature. 1986 Nov 6;324(6092):60-3.
PMID: 12356091 [PubMed - indexed for MEDLINE]2: Bridle JR, Butlin RK. Related Articles, LinksMating signal variation and bimodality in a mosaic hybrid zone between Chorthippus grasshopper species.
Evolution Int J Org Evolution. 2002 Jun;56(6):1184-98.
PMID: 12144019 [PubMed - in process]3: Julian GE, Fewell JH, Gadau J, Johnson RA, Larrabee D. Related Articles, LinksGenetic determination of the queen caste in an ant hybrid zone.
Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8157-60.
PMID: 12034873 [PubMed - indexed for MEDLINE]4: Bierne N, David P, Boudry P, Bonhomme F. Related Articles, LinksAssortative fertilization and selection at larval stage in the mussels Mytilus edulis and M. galloprovincialis.
Evolution Int J Org Evolution. 2002 Feb;56(2):292-8.
PMID: 11926497 [PubMed - indexed for MEDLINE]5: Sasaki A, Kawaguchi I, Yoshimori A. Related Articles, LinksSpatial mosaic and interfacial dynamics in a Mullerian mimicry system.
Theor Popul Biol. 2002 Feb;61(1):49-71.
PMID: 11895382 [PubMed - indexed for MEDLINE]6: Stacy EA. Related Articles, LinksCross-fertility in two tropical tree species: evidence of inbreeding depression within populations and genetic divergence among populations.
Am J Bot. 2001 Jun;88(6):1041-1051.
PMID: 11410468 [PubMed - as supplied by publisher]7: Campbell DR, Waser NM. Related Articles, LinksGenotype-by-environment interaction and the fitness of plant hybrids in the wild.
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PMID: 11392384 [PubMed - indexed for MEDLINE]8: Johnston JA, Grise DJ, Donovan LA, Arnold ML. Related Articles, LinksEnvironment-dependent performance and fitness of Iris brevicaulis, I. fulva (Iridaceae), and hybrids.
Am J Bot. 2001 May;88(5):933-938.
PMID: 11353718 [PubMed - as supplied by publisher]9: Britch SC, Cain ML, Howard DJ. Related Articles, LinksSpatio-temporal dynamics of the Allonemobius fasciatus- A. socius mosaic hybrid zone: a 14-year perspective.
Mol Ecol. 2001 Mar;10(3):627-38.
PMID: 11298974 [PubMed - indexed for MEDLINE]10: Good TP, Ellis JC, Annett CA, Pierotti R. Related Articles, LinksBounded hybrid superiority in an avian hybrid zone: effects of mate, diet, and habitat choice.
Evolution Int J Org Evolution. 2000 Oct;54(5):1774-83.
PMID: 11108604 [PubMed - indexed for MEDLINE]11: Fritsche F, Kaltz O. Related Articles, LinksIs the Prunella (Lamiaceae) hybrid zone structured by an environmental gradient? Evidence from a reciprocaltransplant experiment.
Am J Bot. 2000 Jul;87(7):995-1003.
PMID: 10898777 [PubMed - as supplied by publisher]12: Alarcon R, Campbell DR. Related Articles, LinksAbsence of conspecific pollen advantage in the dynamics of an Ipomopsis (Polemoniaceae) hybrid zone.
Am J Bot. 2000 Jun;87(6):819-824.
PMID: 10860912 [PubMed - as supplied by publisher]13: Castiglia R, Capanna E. Related Articles, LinksContact zones between chromosomal races of Mus musculus domesticus. 1. Temporal analysis of a hybrid zone between the CD chromosomal race (2n=22) and populations with the standard karyotype.
Heredity. 1999 Sep;83 ( Pt 3):319-26.
PMID: 10504430 [PubMed - indexed for MEDLINE]14: Alibert P, Renaud S, Dod B, Bonhomme F, Auffray JC. Related Articles, LinksFluctuating asymmetry in the Mus musculus hybrid zone: a heterotic effect in disrupted co-adapted genomes.
Proc R Soc Lond B Biol Sci. 1994 Oct 22;258(1351):53-9.
PMID: 7997458 [PubMed - indexed for MEDLINE]15: Barton NH. Related Articles, LinksThe effects of linkage and density-dependent regulation on gene flow.
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PMID: 3804768 [PubMed - indexed for MEDLINE]16: Shaw DD, Wilkinson P, Moran C. Related Articles, LinksA comparison of chromosomal and allozymal variation across a narrow hybrid zone in the grasshopper Caledia captiva.
Chromosoma. 1979;75(3):333-51.
PMID: 535498 [PubMed - indexed for MEDLINE]PB:
Thus, the more variability is inbred the closer the organism will resemble the original 'kind' containing all original genetic info.M:Inbreeding reduces variability. More inbred individuals do not look like the last common ancestor or do you think the Amish are more genetically similar to Homo erectus because they are more inbred than the average human population?MY RESPONSE:
Here I also meant crossbreeding.M: Ok, so if I cross two species or subspecies, they should be genetically more similar to their ancestor?....care to show some evidence that donkeys or wolf-dog hybrids are more like their last common ancestor? If an Asian and an African have a kid, are you saying the genotype will be closer to cro magnon? What about all the stabilizing repair enzymes preventing any change backwards or forwards..so much for your hypothesis being the easiest answer to everything.PB: Cro magnon was probably already another subspecies of the human archetype. But, anyway, you show that you are beginning to understand the MPG hypothesis. Your idea is okay.MY RESPONSE:
I already explained how the multipurpose genome works. Preexisting DNA elements induce variability due to differential regulation, and is probably partially irreversibel due to the character of these elements. I guess you would call these elements retroviroids, or LINE's or SINE's. Or whatever you call them.M: Does not look like this holds up either....
BMC Evol Biol 2002 Sep 10;2(1):16 Related Articles, LinksLittle qualitative RNA misexpression in sterile male F1 hybrids of Drosophila pseudoobscura and D. persimilis.Reiland J, Noor MA.Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA. mnoor@lsu.eduBACKGROUND: Although the genetics of hybrid sterility has been the subject of evolutionary studies for over sixty years, no one has shown the reason(s) why alleles that operate normally within species fail to function in another genetic background. Several lines of evidence suggest that failures in normal gene transcription contribute to hybrid dysfunctions, but genome-wide studies of gene expression in pure-species and hybrids have not been undertaken. Here, we study genome-wide patterns of expression in Drosophila pseudoobscura, D. persimilis, and their sterile F1 hybrid males using differential display. RESULTS: Over five thousand amplifications were analyzed, and 3312 were present in amplifications from both of the pure species. Of these, 28 (0.5%) were not present in amplifications from adult F1 hybrid males. Using product-specific primers, we were able to confirm one of nine of the transcripts putatively misexpressed in hybrids. This transcript was shown to be male-specific, but without detectable homology to D. melanogaster sequence. CONCLUSION: We tentatively conclude that hybrid sterility can evolve without widespread, qualitative misexpression of transcripts in species hybrids. We suggest that, if more misexpression exists in sterile hybrids, it is likely to be quantitative, tissue-specific, and/ or limited to earlier developmental stages. Although several caveats apply, this study was a first attempt to determine the mechanistic basis of hybrid sterility, and one potential candidate gene has been identified for further study.PB: I will spell this paper out. At fisrt sight I don’t see a problem here for the MPG hypothesis.PB:
Whether the original kind can ever be backcrossed remains to be established. My guess is NOT, since regulatory elements like retroviruses may have an irreversible effect on gene expression. So, in my opinion, the original genome is plastic within preset limits.M: To bad this is not a testable hypothesis...preset by whom?PB:
As if evolutionism is a testable hypothesis. It has been tested and falsifies over and over.
Preset by the multipurpose genome, of course. The Creator if you like.M: Besides your desperate attack on evolution you did not answer actually respond to this...what is the testable hypothesis? But thanks for your candor in eliminating the multipurpose genome from the realms of science and properly designating it as a religion (an interesting one granted).PB: The predictions made by the MPG hype can be tested. See mail #1 for predictions and falsifications.PB:
Alleles of what? Regulatory networks? Immunogenes? Genes coding metabolism proteins? It all depends on the alleles you are referring to. Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are bot mutant alleles.M: Hmmmm have you ever studied genetics? Are you really really sure that "Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are both mutant alleles"? Ever hear of dominant mutants? Partial dominance? Penetrance? Genetics 101 Peter.MY RESPONSE:
Yep, any idea about the mechanisms underlying dominant mutations, and penetrance?M: Yes I do...you going to answer my question first?PB: Wildtype genes are usually better than mutant genes. The major part of the genes is homozygously present, and reflects this observation. So this statement is not so farfetched. For instance, for Drosophila only approximately 30 % of the D. melanogaster genes is polymorph and only 11 % is heterozygous (Page, D.M, and Holmes, E.C. Molecular evolution. A phylogenetic approach. 1998. Blackwell Science Inc. ISBN 0-86542-889-1, p231).PB:Your explanation does not account for wild type alleles. You also have to consider the fact that monomorphic alleles (homozygous) genes is the rule rather than the exception in any organism studied. So, in my opinion, monomorphic genes cannot be the culprit. Loss of genes can be.M: Funny then that for many genes heterozygosity is very high.PB: That point in the direction of non-random mecahnisms. All in accord with the multipurpose genome.M: Funny that there is no evidence for it...yet Monkenstick could easily find evidence for random mutations...show us your data.PB: Monkenstick’s graph showed nothing related to this subject.PB: The Wollemi pine doesn't demonstrate very little, it demonstrates NO variation. Wanna play the same game as Quetzal, with his distortion of scientific observations?M: I sequenced two mammoths for 350 bp of cytb and they were identical...Oh, I believe in god/Elvis resurrected/creator...my belief in evolution is shattered! Dolly the clone is identical to the animal she was cloned from...Oh no...I have to go re-evaluate everything I ever did...thanks for the eye openerPB: Pretty stable DNA. Guarded by stability ensuring proteins I guess. It is a prediction of MPG hypothesis. Did you also determine the age of the samples? Same location finds?PB: No, it is an evolutionary problem. It cannot be explained by NDT, or the gain of new genes. It can be explained by the multipurpose genome: differntial loss and differential regulation of preexisting genes.M: Okay, then you finally have a testable hypothesis. You can isolate a group of poodles like Fred says and you should get St. Bernards if you agree with his prediction..this is not a predicition of evolutionary theory but obviously one of multipurpose-ism.MY RESPONSE:
No, it is YOUR prediction and based upon lack of understanding of the hypothesis of the MG. The actual prediction made by the MG is that due to lost genetic sensible-sequences --not due to genetic monomorphism as you may think-- it is impossible to get St Bernards, or backcross a wolflike animal. However, if you artificially select certain dogs you will be able to generate a wolflike animal from the complete gene pool of the subspecies of dogs. Thus, you bring together all genes that are still present in the gene pool in one organism. Next, you can start breeding with this 'restored multipurpose genome' and you can get the St Bernard, the poodle, the dachshund, the chihuahua, etc.M: Ah, so you don't think dogs are diploid either..or sexually reproducing. Storks bring them to? Earlier you said you could cross breed animals to get an ancestor..now you say you cannot. Interesting that suddenly your entire theory needs natural selection whereas beforer it was pure non-random pre adaptation...PB: Yeah the stork is also included in the multipurpose genome. Not as baby deliverer, however. No, it does NOT require natural selection. Here you refer to artificial selection. As should be obvious, artificial selection can not be compared to natural selection, since it involves intelligence (human intelligence).PB: Non-random mutations have been demonstrated but every time evolutionist provide fallacies to overcome them.M: If by demonstrating you are wrong is how you define fallacy then so be it. Monkenstick at least provided a graph..let's see yours.PB: How can I back up my new hypothesis with peer reviewed science papers that are always discussed subject to evolutionism. As soon as I start to explain the data subject to another paradigm, you start to object. However, I already discussed the ZFX region in this forum with NO response at all. To explain the data between the specis it absolutely requires NON-RANDOM mutations. None of the evo-explanations can hold (as discussed). Likewise, the redundant alpha actinin genes. (I will respond to your comments in mail 64-96 soon)MY RESPONSE:
I commented on his graph. What I meant is the comments of evolutionists in response to the adaptive mutations of Raddman (mail#52 mol. gen. ev. against random mut. thread). It demonstrates that evolutionists overbluff Raddman (a molecular biologist) by their assertions that "..the error prone polymerase has been selected for their ability to allow cell to cope with damage; the generation of variability [in the genome due to this error prone polymerase] may simply a non-selected byproduct". Well, dear evolutionists, do you really understand biology? I have the feeling that they don't, since it makes the polymerase redundant and since they are not under selective constraint evolutionism predicts highly variable DNA sequences with respect to redundant gene. Based on the MG, I predict that knocking out the errorprone polymerase doesn't effect the organism at all. So here you have another problem.
Contrary what evolutionists believe and propagate as fact, molecular biology is not in accord with evolutionism.M: Um, so now you think that if you remove DNA polymerases from an organism it will survive? Have fun trying to generate that mutant strain. And please list the full quote and context for the quote you have posted. As you have it written it really does not make much of a point...and if non-random mutation is so obvious why can't you provide just simply something equivalent to Monkenstick's post?PB: I am talking about the alternative error prone polymerase. I am sure that it can be removed without affecting the organism. I guess, it is a redundant gene.PB:
This is also clear from the Cairns excerpt in letter #52 in the "mol gen evidence against random mutaion thread" (Dr Page response to Fred). Let's have a look at this paper again and I will demonstrate where the evolutionist's reasoning goes wrong. I don't understand that it is not seen through by the molecular biologists involved.M: Let's have a look at some of my and Quetzal's unanswered questions to while we are at it.MY RESPONSE:
As mentioned before, I will answer (and rebut) all your questions. Easy, since evolutionism is false.M: It does not appear to be so easy since you have not convinced any of the evolutionists on this board of anything...but keep trying.PB: Paradigms shifts do not come overnight.Best wishes,
peter[This message has been edited by peter borger, 11-07-2002]

Dear Quetzal,You write that you like to have response to these points:You:
This is rapidly becoming pointless. You have just expended slightly over 8000 words calling me ignorant. Not much of a debate. So in the interests of brevity, I think I’ll simply synopsize.You:
1. You have presented on this thread a claim that you have falsified evolutionary theory. You present as evidence a single organism, Wollemia nobilis, with descriptions and discussion culled from a popular science book rather than anything in any of the scientific literature, as proof that all of biology is incorrect, and that only you have the true answer — a multipurpose genome created by something you call creaton waves (or variously particles). You have, however, not actually provided any evidence that either of these exist, merely repeated assertion that they explain all biological phenomena, and that anyone who doesn’t immediately accept your explanation is willfully blind or ignorant.My response:
I already recommended to read all my threads. I gave several examples that cannot be explained by evolutionism. Either they violate NDT or the violate molecular evolutionary mechanisms. If you don't see that, I once more to recommend to buy a recent book on molecular evolution or molecular biology. (This is not meant as a personal attack , it is an advice. For free, even).You:
2. You have been presented with numerous references calling in to question your use of this organism. To recap, you have been provided the following:Hogbin PM, Peakall R, Sydes MA, 2000. Achieving practical outcomes from genetic studies of rare Australian plants, Aust. J. Bot. 48, 375—382Peakall R. 1998. Exceptionally low genetic diversity in an ancient relic, the Wollemi pine: implications for conservation theory and practice. 45th Annual meeting of the Genetics Society of Australia. Abstracts 86.Setoguchi, H., Osawa, T.A., Pintaud, J.C., Jaffre, T. & Veillon, J.-M. 1998. Phylogenetic relationships within Araucariaceae based on rbcL gene sequences. Amer. J. Bot. 85: 1507-1516Hanson, L. 2001. Chromosome number, karyotype and DNA C-value of the Wollemi Pine (Wollemia nobilis, Araucariaceae). Bot. J. Linn. Soc. 135: 271-274Chambers, T.C., Drinnan, A.N., McLoughlin, S. 1998. Some morphological features of Wollemi Pine (Wollemia nobilis, Araucariaceae) and their comparison to Cretaceous plant fossils. Internat. J. Plant Sci. 159: 160-171My response:
What do these references tell you? Low or No genetic variability? It is interesting that only Peakalls abstract is directly on the topic. You simply avoid to give a straightforward answer. So I will do it once more for you: All sequences analysed show NO variability, while the two (or three) populations are not clones. That was my point. It clashes with molecular evolutionism. As mentioned, it is just another falsification.You:
3. Rather than addressing the specifics of these references — nearly the entire published literature on Wollemia — you have either referred back to the popscience book with which you started the thread, or quibbled over semantics (low vs no variability in Peakall 1998, for example). You have given no indication that you’ve actually read the references. At the same time, you have consistently stated that you — and only you — are capable of correctly interpreting the molecular data whenever anyone has called into question your interpretation. I would note that thus only you are capable of seeing how it supports your theory.My response:
The book by Woodford contains dialogues of Woodford and Peakall one wouldn't find in evolutionary peer reviewed journals (for the obvious reasons). If Peakall wouldn't have agreed with the content these passages would have been left out. Since they are in the book as quotations, I is reasonable to assume that Peakall stands behind his words. Don't you think so?You:
4. When provided alternative explanations for the low (or no, if you prefer) variability in this organism, you have merely hand-waved them away, with statements such as Because there is NO evolutionary explanation. You are free to think that you have provided an explanation, but I know better from a molecular stance. And You (and a lot of other evolutionists) have been so brainwashed that you (they) are unable to think beyond the paradigm of evolutionism. I know your explanations. They do not make sense in the light of molecular evolutionary rules. I explained that several times. You don't listen. You have, unfortunately, failed to state at any time why the mainstream explanations are wrong — merely asserting ever-more vituperatively that they are.My response:
The offered alternative explanations do not explain the total absence of variability within regions where Peakall expected to find them. I qouted Peakall on this subject. Ask Peakall how he feels about it, now. It is you who is doubting his words. Not me. I believe what Peakall says about the tree. That "evolutionism isn't sitting well".
In other words: the tree violates evolutionism.You:
5. You have questioned the basic concepts of population genetics, ecology, etc, with statements such as Population genetics is the field of multipurpose genome and allele frequency variation, not the field of evolution. Nothing evolved here, just variation with respect to preexisting alleles in the gene pool. Such statements bring into question your knowledge of the subject you are attacking. When you’ve been called on it, you have stated that you don’t accept evolutionary explanations, and restate your multipurpose genome assertion — again without supporting documentation.My response:
You still don't understand that the MPG hypothesis is almost similar to evolutionism except that it includes creation. That is your point. You don't want to include creation. My guess is that you are an atheist, since 'theistic evolutionists' cannot object to the MPG hypothesis. (Note that this is not meant as an offence, you are free to be an atheist. I don't mind, as long as you don't propagate evolutionism as fact).You say:
6. You have introduced a number of tangential issues (Il-1, alpha actinin, ZFY/ZFX, cheetahs, etc) and in nearly every case have been provided literature citations showing you are incorrect. You have consistently refused to even discuss the literature, let alone admit that you might have been mistaken, instead relying on simply repeating your original assertion.My response:
These examples still stand as violations of evolutionism (I didn't introduce the cheetah). None of them have been rebutted. You are free to believe that Dr Page or Mammuthus did that, but they didn't. The didn't even come close. As mentioned in a previous mailing, the best defender of evolutionisms I ever met, Dr D. Theobald (talk origins), wasn't able to rebut it either. Nor was Dr R. Page (author of the book Molecular evolution, a phylogenetic approach). The evo-claims on this topic can be readily checked in the genome, nowadays, and that turns out to be the death blow of evolutionism. So, your above claim that I present the wollemi pine as evidence agaisnt evolutionism is not entirely correct. It is ignoring of all my mailings.You:
7. Any time you have made an assertion and been provided an explanation as to why the assertion is incorrect, you retreat to either a repetition of the assertion, ad hominem, or simply ignore the explanation. Here’s one example:quote:
--------------------------------------------------------------------------------
Q: I also agree that Wollemi Pine isn’t an exception — just an extreme example of a normal distribution. As far as variability is good, although a gross oversimplification, in essence this is true. It’s the key to your question above concerning disease susceptibility. I’m surprised I have to explain this basic concept. The more genetically homogenous a population, the less likely it will contain adaptive variants able to survive or take advantage of new selection pressures. IOW, introduce a new pathogen into a population with lots of variation, there’s much more likelihood that there will be some individuals in the population with at least partial resistance to the pathogen. In a homogenous population, the odds of having an individual or group with resistance is much less, and hence if a pathogen effects one individual, it will effect ALL the individuals in the population.
PB: I also agree that the Wollemi pine is an extreme. Namely the extreme of the multipurpose genome. It is able to fight off pathogens due to the preexisting information in the MG.--------------------------------------------------------------------------------Simple re-assertion. No discussion. No argument.My response:
That's the usual way of discussion in evo-literature: Just-so stories. I thought you --as an evolutionist-- would be content with such just-so explanations. But, you are not. Maybe you can understand people better now who are confronted with such meaningless evo-just-so-stories all the time. (It's bit like the up-side-down world now, isn't it?)
However, the wollemi pine is indeed an extreme of the MPG hypothesis, since usually a bit of variation is expected through entropy on neutral positions. But, apparently this extreme tree has such superior DNA repair mechanism --since they never degenerated-- that its DNA doesn't change at all. In accord with MPG predictions.You:
8. You have shown an amazing inability to research or look up standard materials in the normal fashion, rather insisting that your opponents provide the basic references for YOUR assertions (c.f. the horseshoe crab). Find your own damn references.My response:
You have shown an amazing inability to look beyond evolutionary paradigms, even if I mail the one falsification after the other of this outdated theory. In my opinion, my inability to research and to look up refernces is not reflected in my ability to rebut all evolutionary claims. Including yours.You say:
9. Finally, when your arguments have shown to be spurious, you retreat to little more than massive, repetitious ad hominem attacks — such as your last post.My response:
You told me in another thread (on the mtDNA) that you were unable to interpret these data since you had no molecular evolutionary background. I recommended you to read on this highly interesting field of biological science, so you can judge for yourself where evolutionism is smashed by molbiol.You:
In essence, Peter, you have failed. You are reduced to attacking me
personally — evidently because I’m not a molecular biologist, which is odd because many of the references quoted were from molecular biologists who quite obviously disagree with you - or arguing in circles. Unless you are able to specifically refute the mainstream explanations you’ve been provided — with references — you no longer have an argument.My response:
In essence, dear Quetzal, it is evolutionism that fails to fulfil the promise of being explanatory in the origin of life, genes and species. Darwin was wrong, you are wrong and evolutionism is wrong. And, if you are offended by some minor things I said about your insufficient knowledge on molecular biology, than my apologies for that. I didn't mean to hurt your feelings.Best wishes,
Peter

Dear mark,You write:Peter,Provide ONE example that hasn't been trounced, or retract this ridiculously overconfident claim. Sheesh.I say:
1) the redundant Src kinase family,
2) the redundant alpha actinin family,
3) the 1G5 gene in D melanogaster
4) the swim reflex in conjunction with the gag reflex in newborn
5) the ancient mtDNA (is still open for discussion)
6) the ZFY region (nobody responded)
7) the ZFX gene/exon
8) the IL-1beta incongruence (and more)
9) the LCR16a gene
10)the wollemi's invariable DNAAnd probably more.You say:
Whilst you're at it, please answer the questions raised here ; http://EvC Forum: scientific end of evolution theory (2) -->EvC Forum: scientific end of evolution theory (2), & at the same time tell me why neutral theory is part of the NDTI say:
I responded already to your comments. You didn't bring any new arguments to the topic.best wishes,
Peter

Dear Monkenstick,You say:
borger, have you ever, in the past, admitted that you were wrong about anything?My response:
I know when a position is untenable. I know when I am wrong, and I know when I am right.You say:
that seems to me to be the root of the problem. Even if someone conclusively demonstrated your claims to be incorrect, (SHOW ME WHERE, AND I WILL RESPOND TO THAT, PB) I doubt you'd concede defeat - its that strange confidence that the insane invariably posess about their pet crackpot theory. Show me the creatons borger.The root of the problem is the hypothesis of evolutionism. It is incorrect as all my examples demonstrated. It is the overconvinced evolutonist who keeps denying that. All I do is emphasise the current problem in evolutionism and provide examples demonstrating it. If evolutionism had been proven beyond doubt this discussion wasn't necessary.Ever met an evolutionist who admitted he/she was wrong? Or that evolutionism is unable to explain a certain problem? I haven't. There is never a problem for evolutionism. Well there are a lot, as demonstrated. As long as it is propagated as fact I will demonstrate the opposite.
Show you creatons? Show me gravitons! Or regarding evolutionism, show me the transitionforms. That would make it a theory!best wishes,
Peter

Dear mark,You say:"And all have been dealt with."My response:
They haven't ALL been dealt with. Some, have been dealt with, but they haven't been rebutted. If the were I would admit it.You may be wielding Occam's rasor, I possess Athena's Owl. best wishes,
Peter

Dear mamumuthus,You say:
Just to point out Peter, I also brought up the Erlandson study of the entire region comparing insertions, deletions, and point mutations and you have not addressed those issues and claiming that the region remains invariant. Sorry, but that is patently false.My response:
The Erlandson study doesn't rebut Dr Kim's observation that the assessed region of the ZFX gene is completly stable. No variability at all, not even at neutral positions.Best wishes,
peter

dear Mammuthus,You wrote:quote:
--------------------------------------------------------------------------------
Originally posted by Mammuthus:quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
dear Mammuthus,
I know these papers and I know the evolutionary vision of the authors. Still this vision is not explanatory. Maybe you could respond on the specific questions to Dr Wagner. That would clear things up and you will --on the side-- prevent evolutionism from falling.best wishes,
Peter--------------------------------------------------------------------------------***********************Hi Peter,
You will have to tell me then why they are not explanatory. You have shown on several occassions profound misunderstandings of the papers,particularly studies of the ZFX/ZFY region so the burden is on you to demonstrate that your arguements are based on a real flaw in the data or arguments of the authors and not on your lack of understanding of population genetics, biochem, and randomness.My Comment:
According to neutral theory at least a couple of mutations would have been expected in the ZFX region gene analysed by DR Kim. Of course, you will not find this in discussion of evolutionary papers. You have to find out for your self from the raw data. Therefore, I mailed Dr Kim for a copy of the paper. He was very kind to send me one, so I could have a close look at their data. The data show NO variation in this region for 20.000.000 years. What kind of evolution is that?
Similar things have been obsrved for the ZFY region in human and great apes. The observations can only be interpreted as NON-RANDOM evolution. I mailed this months ago and never got a response. Percy was the only one with an (irrelevant) remark. The ZFY region is also still open for discussion/rebuttal.PB: 1) Do these data mean that approximately 450 bp changes occurred on neutral positions?M: SORRY PETER BUT NOTHING IN YOUR LETTER INDICATES TO ME WHERE THIS QUESTION COMES FROM. ARE YOU REFERREING TO SOMETHING IN THE ARTICLE?PB: No, I am refereing to the alpha actinin genes in human. The reference is mentioned in the letter. Look it up and we can discuss this topic in detail. I will demonstrate ho it violates evolutionism, you rebut. Okay?PB: 2) Do these data mean that it would take about 10(exp)6 years for 3 random mutation to occur in the duplicated gene? Thus 150 million years for 450 neutral mutations?M: ONLY IF YOU BELEIVE THAT DNA EVOLVES IN A CLOCKLIKE MANNER. I DON'T SO THE ESTIMATE OF TIME WOULD HAVE A TREMENDOUS VARIANCE ATTACHED TO IT. PURELY NEUTRAL LOCI MIGHT EVOLVE IN A CLOCKLIKE MANNER HOWEVER BUT IT IS DEPENDENT ON A LOT OF OTHER FACTORS I.E. EFFECTIVE POPULATION SIZE; MUTATION RATE ETC.PB: So, you don't believ that DNA evolves in a clocklike manner. How does it evolve than? Through punctuated equilibrium, I guess? Sometimes it evolves, sometimes it doesn't? Pretty good theory. Dear mammuthus, maybe you didn't get it yet but according o neutralists DNA is ALWAYS evolving on neutral positions. It is a random phenomenon, they say. Probably you don't agree with the neutralists, and are a selectionist. If so, let me know and we will discuss how these redundant genes were selected than. I will let you introduce neutral selection. PB: 3) Do these data mean that after each point-mutation there was neutral purifying selection? And, what exactly is it? I mean, what exactly is selection on neutral genes?M: I HAVE NO IDEA WHAT NEUTRAL PURIFYING SELECTION IS SUPPOSED TO MEAN. SELECTION OCCURS ON GENES THAT PROVIDE AN ADVANTAGE OR DISADVANTAGE TO THE ORGANISM. NEUTRAL GENES CAN BECOME HOMOGENIZED BY GENE CONVERSION BUT IT IS NOT BECAUSE OF SELECTIVE CONSTRAINT.PB: Selection on redundant genes? If a gene is inactivated in a population it clearly demonstrates that it doesn't have any selective advantage. That's the evolutionary problem with redundant genes, they are in the genome without selective constraints. How many times do I have to reiterate this observation? Also, redundant genes do NOT evolve faster than essential genes. How many times do I have to reiterate this observation?PB: 3a) Is it independent from nearby genes? Independent from the rest of the genome?M: IT DEPENDS. SOME GENES EVOLVE BY CONCERTED EVOLUTION USING VARYING HOMOGENIZATION PROCESSES SUCH AS GENE CONVERSION. BUT THIS IS NOT THE
CASE FOR ALL GENES.Mol Biol Evol 2002 May;19(5):689-97 Related Articles, LinksPurifying selection and birth-and-death evolution in the histone H4 gene family.Piontkivska H, Rooney AP, Nei M.Institute of Molecular Evolutionary Genetics, Pennsylvania State University, 328 Mueller Lab, University Park, PA 16802, USA. oxp108@psu.eduHistones are small basic proteins encoded by a multigene family and are responsible for the nucleosomal organization of chromatin in eukaryotes. Because of the high degree of protein sequence conservation, it is generally believed that histone genes are subject to concerted evolution. However, purifying selection can also generate a high degree of sequence homogeneity. In this study, we examined the long-term evolution of histone H4 genes to determine whether concerted evolution or purifying selection was the major factor for maintaining sequence homogeneity. We analyzed the proportion (p(S)) of synonymous nucleotide differences between the H4 genes from 59 species of fungi, plants, animals, and protists and found that p(S) is generally very high and often close to the saturation level (p(S) ranging from 0.3 to 0.6) even though protein sequences are virtually identical for all H4 genes. A small proportion of genes showed a low level of p(S) values, but this appeared to be caused by recent gene duplication. Our findings suggest that the members of this gene family evolve according to the birth-and-death model of evolution under strong purifying selection. Using histone-like genes in archaebacteria as outgroups, we also showed that H1, H2A, H2B, H3, and H4 histone genes in eukaryotes form separate clusters and that these classes of genes diverged nearly at the same time, before the eukaryotic kingdoms diverged.Proc Natl Acad Sci U S A 2000 Sep 26;97(20):10866-71 Related Articles, LinksPurifying selection and birth-and-death evolution in the ubiquitin gene family.Nei M, Rogozin IB, Piontkivska H.Institute of Molecular Evolutionary Genetics and Department of Biology, Pennsylvania State University, 328 Mueller Laboratory, University Park, PA 16802, USA. nxm2@psu.eduUbiquitin is a highly conserved protein that is encoded by a multigene family. It is generally believed that this gene family is subject to concerted evolution, which homogenizes the member genes of the family. However, protein homogeneity can be attained also by strong purifying selection. We therefore studied the proportion (p(S)) of synonymous nucleotide differences between members of the ubiquitin gene family from 28 species of fungi, plants, and animals. The results have shown that p(S) is generally very high and is often close to the saturation level, although the protein sequence is virtually identical for all ubiquitins from fungi, plants, and animals. A small proportion of species showed a low level of p(S) values, but these values appeared to be caused by recent gene duplication. It was also found that the number of repeat copies of the gene family varies considerably with species, and some species harbor pseudogenes. These observations suggest that the members of this gene family evolve almost independently by silent nucleotide substitution and are subjected to birth-and-death evolution at the DNA level.PB: Thanks for these refernces. If you read these articles properly, you will find ou that concerted evolution was a concept to understand the uniformity of these high abundance genes, for instance the histon genes, TcR genes, ubuiquitin genes. However, it isn't tenable anymore and recently it was replaced by birth and death evolution. It's a meaningless term that doesn't explain anything. It's what you believe in. Explain what you believe in, maybe I can believe in it too.PB: 3b) Does this type of selection take place on the level of the organism? How?M: AGAIN, YOU REALLY NEED TO LEARN SOME POPULATION GENETICS OR AT LEAST GET A GRASP OF WHAT RELATIVE FITNESS MEANS. EVEN IF A MUTATION IS NOT IMMEDIATELY LETHAL; IF IT PUTS THE ORGANISM AT A DISADVANTAGE IT WILL BE SELECTED AGAINST. YES; IT IS AT THE LEVEL OF THE ORGANISMPB: Maybe I don'r read enough about population genetics. But that not the discussion here. Selection against redundant genes? Please explain. The topic was on neutral selection, remember. However, I am very curious to find out about selection against genetic redundancies.PB: 4) Are there identical (=very recently duplicated) genes in known genomes?Annu Rev Cell Dev Biol 2002;18:53-80 Related Articles, LinksGene co-option in physiological and morphological evolution.True JR, Carroll SB.Department of Ecology and Evolution, State University of New York at Stony Brook, Stony Brook, New York 11794-5245, e-mail: jrtrue@life.bio.sunysb.eduCo-option occurs when natural selection finds new uses for existing traits, including genes, organs, and other body structures. Genes can be co-opted to generate developmental and physiological novelties by changing their patterns of regulation, by changing the functions of the proteins they encode, or both. This often involves gene duplication followed by specialization of the resulting paralogous genes into particular functions. A major role for gene co-option in the evolution of development has long been assumed, and many recent comparative developmental and genomic studies have lent support to this idea. Although there is relatively less known about the molecular basis of co-option events involving developmental pathways, much can be drawn from well-studied examples of the co-option of structural proteins. Here, we summarize several case studies of both structural gene and developmental genetic circuit co-option and discuss how co-option may underlie major episodes of adaptive change in multicellular organisms. We also examine the phenomenon of intraspecific variability in gene expression patterns, which we propose to be one form of material for the co-option process. We integrate this information with recent models of gene family evolution to provide a framework for understanding the origin of co-optive evolution and the mechanisms by which natural selection promotes evolutionary novelty by inventing new uses for the genetic toolkit.PB: I checked out this reference. It is a model, a proposal. The authors do not provide a single example that demonstrates that duplication and cooption has been observed. In fact, the redundancy in the alpha actinin genes opposes the whole putative concept of cooption. What I like to see are genes in the human genome on their way to cooption. That is, show me expressed genes (pseudogenes are irrelevant for this concept) that are moving towards genes with a (slightly) different function through selection. A prediction could be that in distinct subpopulations these duplicated genes have accumulated distinct mutations.PB: 5) Is evolution a phenomenon driven by random mutation?
YESPB: Apparently NOT, judging from examples like the alpha actinin genes, the ZFY region, the 1G5 gene, etcetera.M: I am going to let Quetzal have first crack at a response to your post to him but I found several deep flaws in your statements that I will address if he does not.PB: No worries about that.Best wishes,
Peter[This message has been edited by peter borger, 11-10-2002]

Dear Mammuthus,You say:
Interesting Peter...you now had to change your statement from the ZFX region to the "assessed" region of ZFX. Erlandsson did a more thorough study that falsifies your statement...and now you are also demonstrating that SLPx was correct that you were mis-defining the region as you have here backpedalled.....at some point you will be looking at a single base pair of ZFX for support.I say:
It was Dr Kim --the author of the paper-- who talked about the ZFX gene instead of exon and I was a bit sloppy of me not to notice that. Doesn't invalidate my example, however. The nitpicking begins, I presume. You could have saved yourself the mail, since Dr Page already nitpicked on this observation.
However, are you a neutralist or a selectionist?Best wishes,
Peter