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Member Posts: 3945 From: Duluth, Minnesota, U.S. (West end of Lake Superior) Joined: Member Rating: 10.0 |
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Author | Topic: John A. (Salty) Davison - The Case For Instant Evolution | |||||||||||||||||||||||
Minnemooseus Member Posts: 3945 From: Duluth, Minnesota, U.S. (West end of Lake Superior) Joined: Member Rating: 10.0 |
For the record, I pulled the Microsoft document that I quoted in message 1, from the Terry's Talk Origins document area, at:
Microsoft OneDrive - Access files anywhere. Create docs with free Office Online. You need to be registered at the site, to access this. (Note: the above link seems to work for me right now, but who knows if it will work for others) The quoted in message 1 is an exact reproduction (except some formatting) of that document. As such, I think it should stand as is in message 1. Of course, Salty is welcome to submit corrections to it, as new message(s) in this topic. I don't understand why, but the source was atributed to "Cherokee" and not "Salty". Since I pulled the file, I have noticed a "My Documents" folder, by Salty, but there does not seem to be anything in it. Moose
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peter borger Member (Idle past 7696 days) Posts: 965 From: australia Joined: |
Dear Grape Ape,
In response to:-------------------------------------------------------------------------------- salty writes: Information must have a source and there is virtually no evidence that new information has been added during the differentiation of the genera Pan,Gorilla,Pongo and Homo. In fact I can't think of an example demonstrating the addition of meaningful new specific information anywhere. Perhaps someone can enlighten me. -------------------------------------------------------------------------------- GA: I'll be glad to enlighten you, but it's not anything that can't be found by doing a quick PubMed search. Example 1: Birth of two chimeric genes in the Hominidae lineage. quote:-------------------------------------------------------------------------------- How genes with newly characterized functions originate remains a fundamental question. PMCHL1 and PMCHL2, two chimeric genes derived from the melanin-concentrating hormone (MCH) gene, offer an opportunity to examine such an issue in the human lineage. Detailed structural, expression, and phylogenetic analysis showed that the PMCHL1 gene was created near 25 million years ago (Ma) by a complex mechanism of exon shuffling through retrotransposition of an antisense MCH messenger RNA coupled to de novo creation of splice sites. PMCHL2 arose 5 to 10 Ma by an event of duplication involving a large chromosomal region encompassing the PMCHL1 locus. The RNA expression patterns of those chimeric genes suggest that they have been submitted to strong regulatory constraints during primate evolution. -------------------------------------------------------------------------------- PB: this is GUToB rule #3 see here: http://EvC Forum: Defining GUToB -->EvC Forum: Defining GUToB GA's example 2: Accelerated Protein Evolution and Origins of Human-Specific Features. Foxp2 as an example. quote:-------------------------------------------------------------------------------- Genes responsible for human-specific phenotypes may have been under altered selective pressures in human evolution and thus exhibit changes in substitution rate and pattern at the protein sequence level. Using comparative analysis of human, chimpanzee, and mouse protein sequences, we identified two genes (PRM2 and FOXP2) with significantly enhanced evolutionary rates in the hominid lineage. PRM2 is a histone-like protein essential to spermatogenesis and was previously reported to be a likely target of sexual selection in humans and chimpanzees. FOXP2 is a transcription factor involved in speech and language development. Human FOXP2 experienced a >60-fold increase in substitution rate and incorporated two fixed amino acid changes in a broadly defined transcription suppression domain. A survey of a diverse group of placental mammals reveals the uniqueness of the human FOXP2 sequence and a population genetic analysis indicates possible adaptive selection behind the accelerated evolution. Taken together, our results suggest an important role that FOXP2 may have played in the origin of human speech and demonstrate a strategy for identifying candidate genes underlying the emergences of human-specific features. -------------------------------------------------------------------------------- PB: Also GUToB rule #3. GA's example 3: The Tre2 (USP6) oncogene is a hominoid-specific gene. quote:-------------------------------------------------------------------------------- Gene duplication and domain accretion are thought to be the major mechanisms for the emergence of novel genes during evolution. Such events are thought to have occurred at early stages in the vertebrate lineage, but genomic sequencing has recently revealed extensive amplification events during the evolution of higher primates. We report here that the Tre2 (USP6) oncogene is derived from the chimeric fusion of two genes, USP32 (NY-REN-60), and TBC1D3. USP32 is an ancient, highly conserved gene, whereas TBC1D3 is derived from a recent segmental duplication, which is absent in most other mammals and shows rapid amplification and dispersal through the primate lineage. Remarkably, the chimeric gene Tre2 exists only in the hominoid lineage of primates. This hominoid-specific oncogene arose as recently as 21-33 million years ago, after proliferation of the TBC1D3 segmental duplication in the primate lineage. In contrast to the broad expression pattern of USP32 and TBC1D3, expression of Tre2 is testis-specific, a pattern proposed for novel genes implicated in the emergence of reproductive barriers. The sudden emergence of chimeric proteins, such as that encoded by Tre2, may have contributed to hominoid speciation. -------------------------------------------------------------------------------- PB: Again GUToB rule #3. GA: These are just a few examples of unique genes within human beings (many more will be found when Pan gets sequenced). PB: The genes you call unique have been derived from preexisting DNA elements, as predicted by GUToB. In addition, it is highly unlikely that such genes arrived by random muations and selection (one can calculate a bit on it) and thus I advocate a non-random mechanism. Indeed, mechanism for non-random mutations (NRM) have recently been described. For an overview of NRM see Caporale's book "Darwin in the genome" and (almost) all my threads. GA: You're saying that all "information" was already there prior to the divergence of Homo, Pan, Gorilla, etc.. So where did the new ones in Homo come from? PB: You didn't get it. Functional DNA elements do not just drop out of the sky (that would falsify the GUToB). The 'novel' genes have been derived from preexisting DNA elements and are most likley re-assembled through NRM. Probably, there are gene-generating mechanisms in the genome. GA: It seems to me that your claim about new "information" is easily refuted by two commonly observed phenomenon in comparative genomics: 1) The tendancy for novel genes to exist uniquely in some species, but not in any closely related species (PMCHL1, PMCHL2, and Tre2 are a few examples from above.) Please note that if you're going to claim that the other species lost this gene from the original "information", then you're talking about multiple parallelisms. There is also clear-cut evidence for recent origin in many of these cases. PB: If the genes are really novel you would be right. But they are not. They are derived from preexisting DNA elements. It is GUToB rule #3. The recent origin of such genes make it highly doubtful that they arose through a random mechanism. For instance the gene in the LCR16a segment (Johnson et al, Nature 2001, 413;514-19). GA: 2) The tendancy for homologous genes to have different sequences and functions in closely related organisms (FOXP2 from above). Clearly an example of new information. PB: It is derived from preexisting DNA elements. Probably through NRM. GA: Starting with "A" in a common ancestor and then ending up with "A" and "B" in its descendants is about as clear-cut as it gets. So both paralogues and orthologues have to be accounted for. PB: The duplication-divergence mechanism sounds reasonable but cannot be the origin of the members of the Src-phosphatase family: point mutations give non-viable phenotypes (while knockouts are viable). In fact this family falsifies the evolutionary vision. GA: Now either it's obvious that new information has arisen since the common ancestor of the great apes, or you're using a definition of information that's not biologically relevant. Using the two most common definitions of information as used by information theorists (Shannon information and Kolmogorov-Chaitin complexity) it's been demonstrated that mutation and selection are perfectly capable of increasing information. If you're using "information" differently, then you'll have to give it a rigorous definition, show why it can't (or hasn't) increased, and explain how it's relevant to biological organisms. PB: My still unaddressed question I've asked almost a year ago: When a functional redundant gene is knocked out is there a loss of information? It should be noted that redundant genes do not have an association with gene duplication and do not mutate faster. (in: A genetic uncertainty problem by D. Tautz, TiG 2000; 16:475-7) GA: As far as I'm concerned, the only relevant metric of information -- that is, the addition of functional complexity (akin to Kolmorgorov-Chaitin complexity) -- can easily be shown to have increased by the above examples. And there are many others, some of which you can find here. Please note also that many of these novel genes have tell-tale signs of recent origin, especially the retrogenes. PB: Apparently biological information can not be defined that way, since non-phenotype knockouts are rather the rule than exceptions. GA: What's ironic here is that most ID-types claim that new information has been added but that mutation and selection are somehow incapable of doing the job. It really can't be both. You can't both have new information, but no way of getting it, and then have no new information. Of course neither one is true. But it's always fun to see mutually exclusive claims coming from the ID camp. PB: What is the selective constraint to keep redundancies stable in the genome? Best wishes,Peter
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Admin Director Posts: 13046 From: EvC Forum Joined: Member Rating: 2.7 |
Hi Peter,
As I already said in Message 300 of the Where is the evidence for evolution? thread, until such time as we have a clear definition of GUToB, discussion of it is restricted to the Dr Page's best example of common descent explained from the GUToB. thread. In your message you repeatedly say, "this is GUToB rule #3", but in the concise definition we're trying to develop in the Defining GUToB thread there is no "rule #3". So let's complete the definition so that people can know what you're talking about. And please keep in mind that no matter what definition you use, bare assertions like "this is GUToB rule #3" with no elaboration is a violation of the guidelines. --------------------EvC Forum Administrator
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peter borger Member (Idle past 7696 days) Posts: 965 From: australia Joined: |
dear Admin,
Since I've set up the GUToB myself I do not need your agreement on it. GUToB rule #3 holds: 3) mechanism for adaptive phenotypes and variation are preexisting in the genome and are due to duplication and/or shuffling of preexisting DNA elements —-either genes or other non-coding elements-- that affect gene expression, or due to loss of (redundant) genes, and through RNA editing. Rule #3 predicts that novel genes are always related to and derived from preexisting DNA elements. Best wishes,Peter
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Admin Director Posts: 13046 From: EvC Forum Joined: Member Rating: 2.7 |
Hi Peter Borger,
Since I've set up the GUToB myself I do not need your agreement on it. Okay, if you say so, but I need you to work with me, not against me, to help keep discussion on track. Think about it over the next seven days during your one week suspension of posting privileges. --------------------EvC Forum Administrator
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Mammuthus Member (Idle past 6506 days) Posts: 3085 From: Munich, Germany Joined: |
Hi Admin,
While I do understand why you suspended Borger, isn't seven days a bit harsh? Though I disagree completely with both salty and Borger on just about everything they post, I still would like to interact with them. It would be a pity if Borger used this as a justification to say all evo's are horrible and therefore his ideas are justified and he need never explain his GUToB to you or anyone else. His response to you was completely stupid...but maybe make him go stand in a corner with a dunce hat on for the weekend rather than a week. By the time 7 days elapse (if he comes back at all) I really doubt he will address the issues you wish to discuss. More likely he will be bellicose and get himself banned out fo frustration. Okay, I can see a good spamming coming from SLPx and others for defending PB
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Mammuthus Member (Idle past 6506 days) Posts: 3085 From: Munich, Germany Joined: |
However, bacteria and viruses DO exchange information very frequently via conjugation and recombination...so should this be the psuedo-semi-hemi-meiosis theory?
By the way, how does your statement that only chromosomes can be responsible for evolution explain the four fold reducition in mtDNA and nuclear genes of humans versus Pan, Gorilla, and Pongo? or Foxp2, the reduction of olfactory genes in humans versus other primates,or syncytin and the establishment of syncitiotrophoblast fusion via an endogenous retroviral envelope gene that is specific to Old world Monkeys through humans but absent in all other taxa etc etc.
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Quetzal Member (Idle past 5902 days) Posts: 3228 Joined: |
Hi Salty,
Sorry I didn't get a chance to get back to you sooner.
Salty writes: With respect to karyotype differences in mice, I specifically indicated in the Manifesto that all such rearrangements need not result in speciation. I'm aware of what you wrote in the Manifesto. That wasn't the thrust of my question. I was not discussing speciation OR primate phylogeny. I was specifically asking for clarification on your statement (from the OP): "The reorganization of a chromosome is an all-or-none event for which intermediate or gradual stages are inconceivable." The clarification seems to be required because observation of different karyotypes within species - which can justifiably be considered intermediate and/or gradual stages of pre-speciation through allopatry - would appear to disconfirm a major assumption of your theory. Especially if there is evidence that karyotypes can and do recombine where clines overlap as was demonstrated in the well-studied M. musculus references I cited. Sorry if I wasn't clear.
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John A. Davison  Inactive Member |
I was referring to the event itself. All genetic changes are of course all-or-none events. The uncomfortable fact remains that sexual reproduction apparently can't produce clear unambiguous species. Rodents are a very old taxonomic unit like Drosophila. Apparently macroevolution was completed a long time ago. Again, these ideas are not new with me, but were suggested by Broom, Huxley, Petrunkevitch and Grasse (some of my heroes). salty
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John A. Davison  Inactive Member |
I specifically indicated in my Ontogeny paper that the information for both ontogeny and phylogeny may have been present from near the beginning of each process. I also indicated that "something or someone must have put it there" or words to that effect. Information must have a source. I also repeat my conviction that there is no evidence that chance has played a significant role in organic evolution, just as it plays no significant role in development. I have even asked the question "has evolution been guided". I guess that makes me a vitalist of sorts, sort of like Louis Pasteur. Again, my ideas stem from those of several of my predecessors, for whom I have profound respect. salty
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Mammuthus Member (Idle past 6506 days) Posts: 3085 From: Munich, Germany Joined: |
So the mammalian radiation that lead to the generation of all the exisiting orders of mammals was produced asexually but then each line independently became sexually reproducing with homologous sex determining pathways and evolution ceased? The incredible species diversity of cichlid fish was from an asexual species and then each spontaneously became sexually reproducing? Or please point out the asexually reproducing primate that yielded chimps and humans and please also provide your compelling evidence for this extremely unparsimonious explanation.
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Mammuthus Member (Idle past 6506 days) Posts: 3085 From: Munich, Germany Joined: |
"I also repeat my conviction that there is no evidence that chance has played a significant role in organic evolution, just as it plays no significant role in development"
This is a real gem! Chance plays no role in devlopment??? Then explain X chromosome inactivation, developmental abnormalities, phenotypic variation i.e. coat color variation in clones, and on the topic of clones, why is it difficult (hint: has to do with chance), Differences in phenotype and behavior in monozygotic twins etc. etc. etc.
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John A. Davison  Inactive Member |
Dear Mammuthus, Since you refer to my hypothesis as the "pseudo-semi-hemi-meiosis theory", I don't feel compelled to respond to you. If you can offer a question free from your obvious prejudice, I may respond. salty
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John A. Davison  Inactive Member |
You obviously overlooked the word "significant". salty
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Mammuthus Member (Idle past 6506 days) Posts: 3085 From: Munich, Germany Joined: |
Are you really that sensitive about the name of your hypothesis or are you ducking all of my questions? Didnt you after all in your Manifesto thank those who stood against you i.e. the administrator who docked your salary and pulled you out of the classroom for re-enforcing your determination to face off "Darwinists"
Regardless, it is your choice whether you respond to the points I brought up or not...I already know the scientifically supported answers. I await (though it is likely futile) your evidence, experimental or otherwise. cheers,M
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