molecular genetic evidence for a multipurpose genome

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Originally posted by mark24:
Fred,

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Since evolutionists generally reject a thorough definition of information (since it refutes their theory), for the sake of discussion we can limit the definition to the following: An algorithm that programs something that is useful for the organism’s gene pool. We’ll assume the sender is nature (as opposed to the obvious choice of intelligence). That is, we’ll already assume that nature (via blind selection and chance mutation) created the algorithms (aka genes) in the parent population. I’m already giving you a huge (realistically unbridgeable) head start.

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Welcome back, Fred, glad you brought this up. Could you continue with this thread please. I believe Percy is waiting for a response, as well.

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http://EvC Forum: Information and Genetics

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1/ Let’s get back to the crux of the argument, does evolution require naturally arising new information in the genome?

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2/ Does evolution require naturally arising information that never previously existed in the genome?

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What’s the bloody difference, except for a definitive one? You have tried to say evolution can’t occur because, 1/ can’t occur. If this were actually a physical restraint, you would have a point, but since scenario 2/ CAN be true, evolution is safe from information theory.

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Thanks,

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Mark

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What is that we hear? The sound of silence
Don't hold your breathe for an answer Mark

FW:
Where do you think I misrepresented you? Perhaps here:M previous post:
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.FW:
Don't you know that populations evolve, not individuals? M: Which part or parts of these sentences from my above quote do you not understand or wish to misrepresent? "However, the cheetah population as a whole has less variation. That is the consequence of a genetic bottleneck"FW:
Seriously, it sure seems you implied, and still are implying, that the cheetah population (its gene pool) has the same amount of genetic information as the pre-bottleneck parent species.M: Which is exactly why you misrepresented what I said. I specifically asked Peter if he was suggesting a Lamarkian (i.e. pre adaptive mutation is what he believes in i.e. multipurpose genome) or that cheetah's somehow lost a part of their "multipurpose" genome.FW:
If the cheetah lost a net sum of ONE useful allele from the parent population then it is patently obvious that its gene pool has LESS genetic information than the parent species. Do you agree or disagree with this?M: Did not say I disagree and in the paragraph above I state this though you ignored it. I disagreed with a Lamarkian mechanism where mutations occur non randomly to pre adapt an organism to novelty i.e. Borger's hypothesis. And as I said, individual cheetah's today have as many genes as each other and their ancestors give or take retrotransposition events. They have less alleles in the population. If you had actually READ what Peter and I were discussing you might not be so confused.FW:
The analogy was an attempt to illustrate the impact on the gene pool after a bottleneck. Bottlenecks are a sure-fire way of producing a new sub-population whose gene pool will have less genetic information than the original parent population. Your claims regarding the cheetah clearly implied that you do not think this is the case.M: This was not your analogy. You were claiming that I believed isolating poodles would lead to generation of St. Bernards which is patently false....my question to Peter was if he believed all possible variation occurs in an individual which is Lamarkian and wrong. He claimed the cheetah has poor genetic content which is also false. It is not extinct so calling the content "poor" is an inappropriate valuation. That YOU apparently believe that isolating one dog breed leads to generation of another specific breed is your confusion, not mine.FW:
Your point is only valid if Peter or I had questioned the existence of random mutations. We have not done this, so your above statement is a classic strawman. You still seem to be the only one on this board who fails to recognize your "good one" was nothing of the sortM: My point remains valid. You have yet to support your assertion of non-random mutation. Monkenstick was able to demonstrate random mutation. As to what others on this board recognize, I would not be so sure everybody is worshipping at your feet there Fred ...that evidence is also lacking.

Since I am not going to get any answers to any of my questions I will jump in here in places but let Quetzal respond in full.I say:
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.M: So cloning does not explain invariability to you?PB:
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.M: Ah so now you think that there are no differences between individuals and that the histones magically guide all development...is this an addendum to your hypothesis. All the sequences tell you is that bottlenecked species that clone have little genetic variation...wow..what a surprise!My response:
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.M: When you make unsupported claims or demonstrate that you don't even know about the basics of the field you are arguing against it makes it hard to take you seriously....it also does not help that you do not answer question regarding your hypothesis.PB:
If it is so common, give me the references please that show NO variability in subpopulations of organisms.M: Take your pick, mice, cows, sheep and cats have been cloned...some have yielded multiple clones.PB:
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.M: If you can't take the heat......PB:......but I know better from a molecular stance.M: Unwarranted conclusionPB:
My response:
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.M: That's a laugher....bottlenecks and founder events can lead to speciation i.e. restriction of genepool I see you have remained immunized against reading Hartl and Clark.PB:My response:
Through jumping/shuffling DNA elements that affect gene expression. Like the 10.000 generations of bacteria-reference of Mammuthus. The authors concluded that single nucleotide polymorphisms was not abundant and cannot have been a major contribution of the observed phenotypic changes. In contrast, jumping DNA elements did.M: Patently false, the authors did not measure the contribution of point mutations as assaying mobile elements was easier.From the abstract of Lenski's paper: Molecular methods are used widely to measure genetic diversity within populations and determine relationships among species. However, it is difficult to observe genomic evolution in action because these dynamics are too slow in most organisms. To overcome this limitation, we sampled genomes from populations of Escherichia coli evolving in the laboratory for 10,000 generations. We analyzed the genomes for restriction fragment length polymorphisms (RFLP) using seven insertion sequences (IS) as probes; most polymorphisms detected by this approach reflect rearrangements (including transpositions) rather than point mutations.PB:
I say:
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'. {But, as mentioned before, there is no junk in the DNA. It is an outdated evolutionary vision. Of course Dawkins still mentions it in his 1998 book that 98% is junk. But he doesn't know better-- he is a zoologists-- so he can be forgiven}M: Too bad for your hypothesis that all of these sequences do vary even among individuals of the same species.PB:
I say:
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.M: Please provide the citations that it is believed by ALL developmental biologists that gene expression is only changed by shuffling of DNA elements. And also please show us where all the papers showing point muations that induce major changes have been retracted.PB:
My response:
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.M: Please then demonstrate human reproduction through copicing. The program must be in there somewhere..or some left over evidence of it.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).M: Sigh...Hartl and Clark...basic evolution texts...ability to interbreed does not mean the two belong to the same species...ever hear of a hybrid zone? Obviously not.Quetzal:
You say:
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.M: Peakall also understands what a clone is...why don't you?Thanks for not answering any of my questions regarding your hypothesis...back to being ignored

FW:
Don’t blame the confusion on me.M: I can and do blame the confusion on you since you are the only one confused here.

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M: My point remains valid. You have yet to support your assertion of non-random mutation. Monkenstick was able to demonstrate random mutation. As to what others on this board recognize, I would not be so sure everybody is worshipping at your feet there Fred ...that evidence is also lacking.

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FW:
It’s amazing you cling to this. Since no one here has denied random mutation, the point is a strawman.M: It is amazing that you cling to mythology like the worldwide flood. And my point is not a strawman. Any way you cut it you have not provided any evidence of non-random mutation yet there is plenty of evidence for random mutation...you can avoid it all you want but this fact does not go away.FW:
But let’s be honest.M: You honest? I'm an atheist..I don't believe in miracles.FW:
Monkenstick thought it somehow showed all randomness and argued against the existence of non-random mutations. I think this is also what you thought when you read his post. But the fact is, it turns out his citation has nothing at all to say about non-random mutations. WHen you realized this, you tried to shift the goalposts and turn it into a strawman. Your choices are not appealing: 1) bogus claim, 2) strawman. There is of course a 3rd choice 3) admit your mistake and move on (I promise I won't gloat, I make my fair share of mistakes)M: It was a good one and I have no mistake to admit. What you should admit is that you cannot demonstrate non-random mutation and are desperately trying to deflect the conversation away from this painful fact.FW:
But since you continue to refuse, you win a special prize. Please go here:How to keep an idiot busyM: Grow up Fred. You claimed you were capable of civilized discussion and yet here you demonstrate behavior befitting a mentally challanged donkey.FW:
I’m curious, are there any evolutionists at all on this board who believe Mams good one point was valid? Come on, don’t be shy. Embarassing to rebut a fellow evo? Man, it’s not even that big of a point to concede on. Anway, if you agree Mams had a point, see above link. Thanks!M: Does anybody out there think Fred has anything substantive to say?

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Originally posted by Fred Williams:
Mark,

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I don't have much time left tonight. Can you post your example of loss of info to save me the time of searching for it. I'll try to respond tomorrow, but I can't promise anything becuase I have to get some work done (I have to get out my brush and do some nvsram scrubbing - hmm, this serves as a prime example of *increase* in information for our product ).

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***********************Fred's latest method of ducking all questions to him...he is too busy..and the dog (oh I mean the poodles he thinks turn into St. Bernards by genetic drift) ate his homework...

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Originally posted by peter borger:
Dear mammuthus,

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I started this thread to elaborate on your questions and how I see a multipurpose genome. So, stop saying that I am ignoring your questions. If you have the feeling I do, please point out what questions you like to have addressed. Make a list, or so. By the way, why should I answer questions within a day or 2 days? This board will be around for a long time and I have other thing to do too. Ultimately I will address all your questions.

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Best wishes,
Peter

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***************I have repeatedly bumped posts in this and other threads without response. We ALL have other things to do. Considering you have continued to post without answering the multiple bumped posts gives the impression you are ducking the questions.cheers,
M

Hi Peter,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? Or do you just mean lost? 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:
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.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.PB: It doesn't matter for structural and metabolic proteins.M: Do you know this or are you just saying this? 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?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? 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. 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 Clark 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?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:
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:
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. 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.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.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? 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??? 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:
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.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. 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.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.PB:
Non-random mutaions 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:
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.cheers,
M

Hi SLPxSLPx
Indeed.... I see that despite your calm and congenial posting style (and I mean that), Fred has gone on the 'attack'. So much for his implication that he is only a jerk to folks that give him a hard time...[quote] M: I have not been so congenial lately And as I have seen, Fred has been unable to answer a single question put to him...he either replies with an insult, claims all questions are a red herring, claims you said something you did not and then says you have to answer based upon his falsification, or claims he is too busy to answer....he has a clear knowledge deficit and does not cover it very well.SLPx:
Indeed. I have probably been a bit too harsh with TB. Unlike Borger, at least he seemed a bit humble and admitted that his interpretations were bible-based.M:
Well, compared to Fred Williams, Borger and TB look like geniuses
TB always makes a good effort and often brings up interesting points....By the way, don't you love how Fred keeps claiming you and I would never dare to contradict each other and then makes appeals to the unseen public for support

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Originally posted by peter borger:
Dear mammuthus,

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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,

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Best wishes,
Peter

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*************Hi Peter,
I don't have to go that far back..I will bump the unanwswered posts again for you here today. Ok?Best wishes,
M

Hi Peter,
Rather than bumping them yet again (which I imagine the Admin would prefer I not do) I refer you to posts 94-96 in this thread which are unanswered and have been bumped before.You can turn to the Creaton thread at your leisure.cheers,
M

Hi SLPxWhat a joke...Just another example of an overemphasis on internet discussion board posts by the cretin, and utter hypocrisy.Posts are, at least mine are, not designed to be easily transferred to a professional manuscript. I write them on the fly - between classes, at lunchtime, those ocasions that I am caught up on my work and have some time to kill... Typos? Lots. Odd sentences? Plenty. Incorrect word usage? Sometimes. Gasp - errors? On occasion.I don't write - or set out to write - impeccable proclamations on science, and I don't expect it of anyone else, either, though it seems pretty obvious that the average creationiost believes their every utterance has scientific merit...M: I also do my responses on the fly. Only on occassion does a creationist post make me go back to the literature to check. Sometimes with TB and sometimes with Borger...that is why I actually enjoy debating them.Most of the rest either don't stick around or are just a source of amusement...especially when they think their every pronouncement is actually something special ...make you think of anybody posting recently about information theory? SLPx:
When I first started posting to these boards (about 5 years ago), ......M: Wow...you have been at this a long time!SLPx:
Too many times did I have multi-page posts gutted or outright deleted.So I said F*** it - why do all that work when the cretin will ignore, obfusate, dodge, twist, or edit and delete? Why not just point out their ignorance? It is easier to do, faster, and one does not have to worry about making errors!M: You should have seen the old CNN evolution forum...there were hundreds of people posting and they regularly deleted posts without warning. But as far as I have seen, that does not seem to happen here.
I also am frustrated by the same thing i.e. you post a detailed response and the person ignores it or claims YOU never addressed their questions.SLPx:
Last time I checked, randall still had numerous errors on his pages, including the ones I pointed out (I had pointed out several more before he tucked tail and ran).M: He can afford to be lazy since the people who believe what he says would not recognize the errors.SLPx
So, not only does the creationist rarely - if ever - 'correct' an error made by a fellow creationist, they actually seem to embrace their idiocy!By the way - I will nbever correct you in public... You do the same for me, OK pal?M: You spelled never incorre...I mean yes I will not correct you in public ciao,
M

M: It was a good one and I have no mistake to admit. What you should admit is that you cannot demonstrate non-random mutation and are desperately trying to deflect the conversation away from this painful fact.
--------------------------------------------------------------------------------FW:
LOL! You hang in there Mams. Don’t give in! Keep fighting! Preserve that ego!M: Actually from all of your posts it is you who is constantly boasting, avoiding questions, and demonstrating profound ignorance...what's the matter Fred, fail out of grad school so your angry at the world FW:
Why has not a single evolutionist come to your defense on this silly breach of logic you have made?M: As opposed to the masses of people running to agree with your statements?FW:
Even if I totally caved and said I don’t believe non-random mutations occur, your point would still be either bogus or a strawman!M: LOL! duck and bob..duck and bob.....your error was to support non-random mutations and now you have to backpedal by all means possible out of supporting your claims..LOL!FW:
Is this really that hard to figure out? What I believe about non-random mutations has nothing to do with your error. Please Mams, tell us how Monkenstick’s citation is evidence against non-random mutation. Answer this one request and perhaps it will solve the simple riddle that seems so elusive to you.M: Ah and distortions from Fred..what a surprise...I did not say Monkenstick's post is evidence against non-random mutation There IS NO evidence for non-random mutation. Monkenstick provided evidence FOR random mutation...when asked to do the same for your position resort to the pathetic posting style you are so famous for...(your only claim to fame by the way).M:
Fred's latest method of ducking all questions to him...he is too busy..and the dog (oh I mean the poodles he thinks turn into St. Bernards by genetic drift) ate his homework..FW:
Hi Mams. I wrote this a while ago for the trolls at the old OCW board: 404 Not Found While you are not a troll or classical evo-babbler, I do think you need to go out on a date or something.M: However, you Fred are a classical internet troll. Up the dosage of Prozac there Fred..your psychosis is beginning to overwhelm you.

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?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.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.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%.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:
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?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.M: I'm obtuse? You might want to actually be sure your statement about mutant genes is true 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.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 X 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:
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.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....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:
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.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.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 babies 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.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.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.
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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.
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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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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.
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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.
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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.
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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.
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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.
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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: 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.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:
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:
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?M: Yes I do...you going to answer my question first?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: Funny that there is no evidence for it...yet Monkenstick could easily find evidence for random mutations...show us your data.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 opener 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:
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.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:
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.best wishes,
M

FW:
Mammuthus apparently confused a lot of people with that statementM: Confusing you is not challenging...you don't even need my help to be completely confused.

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.M: Funny Peter, you have been accusing me and SLPx of mistreating you because we supposedly don't take an "asthma researcher" seriously. In my case, if I thought you were a moron like Fred Williams I would not take the time to respond to you but since I don't think so, I make the effort. Yet in your reply to Quetzal you did not rebut any of his points but attacked him because he is not a molecular biologist. Given your claim to a Ph.D. it is a wonder that you have such a poor grasp of genetics, developmental biology, and clearly don't know what imprinting is (from your post to Quetzal). You also don't know any population biology. Yet Quetzal has repeatedly shown a broader knowledge on all of these issues than you....I would suggest you debate his rebuttals as opposed to just dismissing everything he says...or if you wish to persist, you should not be so hypocritical as to complain about SLPx when you feel he is doing the same thing...whether you realize it or not, Quetzals's mail absolutely spanked your arguments as rather than responding to the points you attacked him...since you keep saying everyone is "Page" like I will be more insulting and say that you were very "Fred William's" like.So, let's get back to the issues or concede that you cannot.Cheers,
M