Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
3 online now:
Newest Member: popoi
Post Volume: Total: 915,806 Year: 3,063/9,624 Month: 908/1,588 Week: 91/223 Day: 2/17 Hour: 0/0


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   molecular genetic evidence for a multipurpose genome
Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 136 of 317 (21662)
11-06-2002 5:16 AM
Reply to: Message 135 by peter borger
11-06-2002 5:02 AM


quote:
Originally posted by peter borger:
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

*************
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

This message is a reply to:
 Message 135 by peter borger, posted 11-06-2002 5:02 AM peter borger has not replied

Replies to this message:
 Message 138 by Mammuthus, posted 11-06-2002 5:30 AM Mammuthus has not replied

  
Quetzal
Member (Idle past 5871 days)
Posts: 3228
Joined: 01-09-2002


Message 137 of 317 (21664)
11-06-2002 5:23 AM
Reply to: Message 113 by peter borger
11-05-2002 6:05 AM


quote:
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.
I gave you the reference, look it up for goodness sake!
quote:
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.
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. 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.
quote:
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.
quote:
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.
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.
quote:
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.
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. 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.
quote:
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.
I did — I referenced several plants, a couple of mammals, etc. Pay attention. If you can’t keep up, take notes.
quote:
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.
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.
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.
quote:
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.
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.
quote:
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.
quote:
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.
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.
quote:
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.
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.
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.
quote:
(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.)
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.
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.
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.
quote:
My response: endstations can indeed go extinct. Either endstations stay unchanged for eons or they go extinct. Could & Eldredge wrote extensively on this observation.
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.
quote:
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.
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.
quote:
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.
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 know
quote:
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.
Now you’re back to denying organisms have a natural history. Oh yeah, I forgot — magical creaton waves poofed them into existence de novo.
quote:
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.
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.
quote:
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?
quote:
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.
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. 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.
quote:
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.
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.
quote:
As demonstrated above, I will. Present the literature if you are so sure.
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.
quote:
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.
Thanks, I’ll decline. I get enough of a rush out of the real world — I don’t need to accept your fantasy.
quote:
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.
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.
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?
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.
quote:
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.
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? 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?
quote:
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).
Great! Your hypothesis is falsified:
Nurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL (1998), Selective sweep of a newly evolved sperm-specific gene in Drosophila, Nature 396:572-575
quote:
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)
Here’s a brand new gene that was formed from bits and pieces of other genes — not a duplication event.
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 291:128-130
quote:
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.
Note the comparison with D. simulans, which has a recent —observed — common ancestor with D. melanogaster and DOESN’T have the gene.
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?
quote:
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).
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. 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.
quote:
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.
See above — way above.
quote:
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.
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.
quote:
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.
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 : 75-81
Willis, JH (1999), Inbreeding Load, Average Dominance and the Mutation Rate for Mildly Deleterious Alleles in Mimulus guttatus Genetics 153: 1885-1898
Colas 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: 3471-3476
Reinartz JA, Les DH (1994) Bottleneck-induced dissolution of self-incompatibility and breeding system consequences in Aster furcatus (Asteraceae), Am. J. Bot. 81: 446-455
Charlesworth D, Morgan MT, Charlesworth B (1992) The effect of linkage and population size on inbreeding depression due to mutational load Genet. Res., 59: 49-61
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.
quote:
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.
How about we see what the actual data says — WHEN IT’S FINALLY PUBLISHED.
quote:
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.
You have once again failed to address this issue in any way whatsoever other than repeating your mantra. Try again.
quote:
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.
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. Your MG thingy is incredibly elastic, depending on what you’re responding to:
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.
quote:
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.
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.

This message is a reply to:
 Message 113 by peter borger, posted 11-05-2002 6:05 AM peter borger has replied

Replies to this message:
 Message 163 by peter borger, posted 11-06-2002 11:54 PM Quetzal has replied

  
Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 138 of 317 (21666)
11-06-2002 5:30 AM
Reply to: Message 136 by Mammuthus
11-06-2002 5:16 AM


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

This message is a reply to:
 Message 136 by Mammuthus, posted 11-06-2002 5:16 AM Mammuthus has not replied

  
Quetzal
Member (Idle past 5871 days)
Posts: 3228
Joined: 01-09-2002


Message 139 of 317 (21670)
11-06-2002 6:52 AM
Reply to: Message 125 by Minnemooseus
11-05-2002 7:37 PM


Yep - you're absolutely correct. Decreased population variability != decreased information content. That's the whole point. Creationists have been babbling about "information" for years. I suppose it sounds good to the rubes...

This message is a reply to:
 Message 125 by Minnemooseus, posted 11-05-2002 7:37 PM Minnemooseus has not replied

  
Quetzal
Member (Idle past 5871 days)
Posts: 3228
Joined: 01-09-2002


Message 140 of 317 (21675)
11-06-2002 7:38 AM
Reply to: Message 117 by Fred Williams
11-05-2002 6:02 PM


Great reply Fred. You and Peter B seem to be vying for who can give the best non-answer to an honest question.
quote:
Quetzal, methinks you have been reading too much of the gobblygook at T.O. Yours is of the recent evo standard creationists are mixing definitions reply. Why don’t you just deal with the definition I gave you? If you prefer, remove the sender comment. What are you afraid of? I even offered you the simplest level of information, Shannon info. You simply cannot make a case that the cheetah has not lost genetic information from its pre-bottleneck parent population.
I'm afraid I don't read or post on TO. Actually, the whole point is you haven't given a definition. Hard to work with a definition that is internally inconsistent, idiosyncratic, and fundamentally inapplicable and worse, conflates three completely different information concepts. Tell you what - since the whole information argument was YOUR red herring, you show us (with appropriate equations) how information is lost in a population after a bottleneck.
quote:
MEGAROTFL! Q, I can’t count the times I’ve been down this road. If it isn’t sand patterns on a beach, or pee messages in snow, or rings in a tree, or arrows shot across a battlefield, or tiles heading for one’s dome. Blah blah blah. These are simply diversions and invariably a big waste of time. Stick to the debate.
So I take it you don't have an answer? Or rather, since you're so conversant with this type of argument, you don't want to pursue it because you're bored with it?
Tell you what, since this is old hat for you, repost one of your old arguments with the accompanying math. After all - you're the one that wants to use "information" in a discussion of ecology and population genetics. You define the information content of the system. You derive the necessary equations, and show YOUR assertion is valid.
I personally consider the whole "information" argument to be a specious waste of time. So unless you can come up with a compelling reason - or mathematical proof of your contention - I think you're simply blowing smoke. Hence the utterly contentless reply you made.

This message is a reply to:
 Message 117 by Fred Williams, posted 11-05-2002 6:02 PM Fred Williams has not replied

Replies to this message:
 Message 141 by mark24, posted 11-06-2002 7:55 AM Quetzal has replied

  
mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 141 of 317 (21676)
11-06-2002 7:55 AM
Reply to: Message 140 by Quetzal
11-06-2002 7:38 AM


Quetzal,
Fred may not have defined "information", but he HAS defined "new information" as it pertains to the genome.
quote:
new information = the presence of a new algorithm (coding sequence) in the genome that codes for a new useful feature.
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 140 by Quetzal, posted 11-06-2002 7:38 AM Quetzal has replied

Replies to this message:
 Message 142 by Fedmahn Kassad, posted 11-06-2002 8:35 AM mark24 has not replied
 Message 143 by Quetzal, posted 11-06-2002 8:36 AM mark24 has not replied

  
Fedmahn Kassad
Inactive Member


Message 142 of 317 (21680)
11-06-2002 8:35 AM
Reply to: Message 141 by mark24
11-06-2002 7:55 AM


quote:
Originally posted by mark24:
Quetzal,
Fred may not have defined "information", but he HAS defined "new information" as it pertains to the genome.
quote:
new information = the presence of a new algorithm (coding sequence) in the genome that codes for a new useful feature.
Mark

He also said this:
quote:
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?
Therefore, if loss of alleles is loss of information, then the opposite is of course true. That really wasn't so hard to falsify his information argument, unless he disputes that new alleles have been produced.
FK

This message is a reply to:
 Message 141 by mark24, posted 11-06-2002 7:55 AM mark24 has not replied

Replies to this message:
 Message 149 by John, posted 11-06-2002 9:17 AM Fedmahn Kassad has not replied

  
Quetzal
Member (Idle past 5871 days)
Posts: 3228
Joined: 01-09-2002


Message 143 of 317 (21681)
11-06-2002 8:36 AM
Reply to: Message 141 by mark24
11-06-2002 7:55 AM


Hmm, okay. However, I think that still begs the question. Consider:
1. At the level of the organism, that means that any mutation, duplication, fusion, recombination etc that results in either an increase in function, a novel function, or greater efficiency internally (in the "environment" of the cell, cascade, or organism's body), OR which generates a beneficial phenotypical change in relation to the particular organism's environment, constitutes "new information". Okay, I can almost buy that. In that case, it's trivially easy to show new information.
2. However, considered at the level of the population (which is the level at which we were arguing), and based on the fact that the "new" algorithm must be "useful" to the population, I don't see how anyone can quantify the effect of a single novel function in the genome of a single individual as "useful" - hence Fred's question is impossible to answer. Even assuming this new individually-useful algorithm gets somehow fixed and becomes dominant in the population over X generations, how can it be determined to be "useful" even at this point unless it has a net effect on the marginal fitness of the entire population? OTOH, if all that is required is that some member of some population - even if the population is represented by a billion individuals - "gains" a new algorithm (as in #1), then again it is trivially easy to state that the population's gene pool has gained (albeit incrementally) an increase in information.
However, I'd be willing to bet any amount of money you'd care to wager that's not what ol' Fred is trying to get at...

This message is a reply to:
 Message 141 by mark24, posted 11-06-2002 7:55 AM mark24 has not replied

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 144 of 317 (21682)
11-06-2002 8:45 AM


But he doesn't know better-- he is a zoologists-- so he can be forgiven}
I will remember this gem....

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 145 of 317 (21684)
11-06-2002 8:54 AM
Reply to: Message 121 by Fred Williams
11-05-2002 6:32 PM


quote:
Originally posted by Fred Williams:
Dear Scott,
I have said all along that informed evos recognize that the only way to get new gentic information naturalistically is via random gene duplication + subsequent random mutation to the new gene that is beneficial to the population. Do you have such an example?
Your pal,
Fred
Yes, you know all about those "informed evos", don't you?
Unfortunatly, you are dodging my questions/challenges, which is no surprise.
Do you consider Kimura an "informed evo"?
I will have to conclude that your inability/refusal to address my questions/challenges is an implicit concession.
In the end, this whole 'new information' schtick is moot.
Address the scenarios I mentioned, and I will address yours.

This message is a reply to:
 Message 121 by Fred Williams, posted 11-05-2002 6:32 PM Fred Williams has replied

Replies to this message:
 Message 160 by Fred Williams, posted 11-06-2002 7:09 PM derwood has replied

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 146 of 317 (21685)
11-06-2002 8:57 AM
Reply to: Message 123 by peter borger
11-05-2002 6:40 PM


delete double post
[This message has been edited by SLPx, 11-06-2002]

This message is a reply to:
 Message 123 by peter borger, posted 11-05-2002 6:40 PM peter borger has not replied

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 147 of 317 (21686)
11-06-2002 8:58 AM
Reply to: Message 123 by peter borger
11-05-2002 6:40 PM


quote:
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!
But tell us all, Pete, what that has to do with referring to an exon as a gene?
And do you have a soure for your definition?
You see, maybe you just don't know better-- you are an asthma researhcer-- so you can be forgiven}...

This message is a reply to:
 Message 123 by peter borger, posted 11-05-2002 6:40 PM peter borger has replied

Replies to this message:
 Message 161 by peter borger, posted 11-06-2002 7:36 PM derwood has not replied

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 148 of 317 (21688)
11-06-2002 9:05 AM
Reply to: Message 128 by Mammuthus
11-06-2002 3:09 AM


quote:
Originally posted by Mammuthus:
M: Does anybody out there think Fred has anything substantive to say?
Do you really need to ask?

This message is a reply to:
 Message 128 by Mammuthus, posted 11-06-2002 3:09 AM Mammuthus has not replied

  
John
Inactive Member


Message 149 of 317 (21691)
11-06-2002 9:17 AM
Reply to: Message 142 by Fedmahn Kassad
11-06-2002 8:35 AM


quote:
Originally posted by Fedmahn Kassad:
Therefore, if loss of alleles is loss of information, then the opposite is of course true. That really wasn't so hard to falsify his information argument, unless he disputes that new alleles have been produced.
I missed that. Take it back so I can say it?
------------------
http://www.hells-handmaiden.com

This message is a reply to:
 Message 142 by Fedmahn Kassad, posted 11-06-2002 8:35 AM Fedmahn Kassad has not replied

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 150 of 317 (21694)
11-06-2002 9:30 AM
Reply to: Message 132 by Mammuthus
11-06-2002 4:24 AM


quote:
Originally posted by Mammuthus:
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
What 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...
What I do expect is that one - on any side of a discussion - realize this and not harp on minutiae.
I can hear the 'rebuttals' now - "Thats all Page does blah blah blah!"
Well, in a sense, I do - but not on one-time statements. I 'harp on' repeated unsupported assertions. I bring up obvious and blatant errors that are never corrected. I reiterate my objections to pompous assertions regarding how 'informed evos' know this and that, when such a claim is idiotic (but repeated). I point out large-scale back-peddaling. Etc...
When I first started posting to these boards (about 5 years ago), I did take the time to 'research' my posts. To fully address the claims of the creationist. But I soon discovered that if I brought up 10 points, creationists would focus on one and claim victory. Or not respond at all. And if the creationist brought up 10 points and I responded to each of them, they would bring up 10 more. I discovered that creationist censors would merrily simply delete posts that damaged the arguments of their friends or heros, or pointed out the incompetence of professional creationists.
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!
Of course, that gets me branded, but I don't care. I don't mind running blocker for those evolutionists out there that were born with much higher levels of patience than I...
But as for this schtick about not publicly chastizing/correcting a fellow evolutionist... that is just plain old projection.
I have been correted many a time, and I have corrected others.
It is the creationist that tends not to do this. Just look at what I recently mentioned - Luke Randall. He came on thr OCW site some time ago, boasting about how he knew evolution was wrong because he had a PhD in microbiology and genetics, and how the human genome had 3 billion codons. Silence from creationists (including Fred). I correct this, and the cretin (Randall) tells me to "get my science straight" before daring to try to correct a creationist scientist. I prove he is wrong, and he gets indignant, I get attacked by creationists for 'scariug away' a real PhD holding creationist.
Later I see that Fred links to Randall's site, rferring to it as "excellent"...
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).
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?

This message is a reply to:
 Message 132 by Mammuthus, posted 11-06-2002 4:24 AM Mammuthus has replied

Replies to this message:
 Message 151 by Mammuthus, posted 11-06-2002 10:17 AM derwood has not replied

  
Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024