John A. (Salty) Davison - The Case For Instant Evolution

SLPx, I do agree with you, but for at least now, I feel the need to let Salty be Salty. I certainly hope that this doesn't cause you to go into the "cranky mode".This is not to say that Salty exempt from disipline, for any future transgressions he might do.Moose

I'm not sure what the problem is. I was referring to the time it takes for a particular genetic change (mutation) to take place. Of course I don't believe that speciation results from the accumulation of micromutations. I believe that speciation results from single transformations of heterozygous chromosome reorganizations into homozygous form as a result of the fact that, in the first meiotic division, the sister (identical) strands always remain together. In short, I believe that organisms do not themselves change, but rather that they produce in single steps new species as their offspring. Please note that all this must be put in the past tense since it apparently is no longer occurring. I know this sounds crazy but "instant speciation" is precisely what the semi-meiotic hypothesis predicts. I hope this helps. salty

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I was referring to the time it takes for a particular genetic change (mutation) to take place.

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And of what relevance is that to whether or not 'Darwinism' has merit?

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I know this sounds crazy but "instant speciation" is precisely what the semi-meiotic hypothesis predicts.

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Yes, that does sound crazy. How do these mutations - which take a few seconds to physiucally occur in the germline - persist if not by spreading throughout a population?[This message has been edited by SLPx, 03-20-2003]

I don't know where someone got the idea that I am protected by Ilion or Terry. Ilion recently banned me. Apparently he doesn't care for evolutionists of any stripe. As for Terry, I don't think it is very charitable to pick on Terry. Terry has been a very civil and tolerant manager of the Forum. As a matter of fact, I think I may be able to ultimately convert Terry to my Creationist/Evolutionist brand of science. In any event, Terry, at my suggestion, added OR BOTH?? to the title of the forum! salty

I agree that the notion of information being present from the beginning of evolution does seem like magic. That does not mean that it is magic. Is it any more magical than the obvious realtiy that all of the information necessary to produce a unique human being is contained in a single cell, the fertilized egg? I don't think so and Robert DeHaan and Phillip Engle agree with me. Also, if I have now earned the right to be insulted, lay on. I'm a tough old bird!! salty

If these organisms really do use the mode of evolution you propose is there any evidence that they do produce the macromutations that your hypothesis depends on ?Indeed is there any clear evidence that chromosomal rearrangements do produce useful macromutations ? Your manifesto doesn't seem to include any clear and definite evidence that chromosomal rearrangements rather than, say, mutations to regulatory genes are responsible for major phenotypic changes.

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I agree that the notion of information being present from the beginning of evolution does seem like magic. That does not mean that it is magic.

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And yet you have offered no explanation whatsoever about where this 'original' information came from. Do you have one?

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Is it any more magical than the obvious realtiy that all of the information necessary to produce a unique human being is contained in a single cell, the fertilized egg?

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That is not magic. That is simple biology. That 'information' comes form the two parents. That is hardly analogous to where the 'original' information came from. On this, you are empirically silent.

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I don't think so and Robert DeHaan and Phillip Engle agree with me.

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And the fact that you and two "Intelligent Design" advocates agree is supposed to mean what, exactly? This reminds me of Dembski boasting about all of the accolades on his books' dust jackets. Looking at them, they are all from Discovery Institute fellows (to which Dembski belongs).

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Also, if I have now earned the right to be insulted, lay on. I'm a tough old bird!!

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Marginalized because of your obvious dearth of knowledge of the field of evolutionary biology, yes, insulted, no. I'm afraid that is your area of expertise.

The need for sexual reproduction to appear independantly in many lineages is a definite problem for your hypothesis. And I would suggest that it is one of the reasons it is not taken as seriously as you would like. I think that you would be better employed in working out the answers to basic problems with your hypothesis, such as this, rather than making poorly worded attacks on the mainstream view.

I'll be glad to enlighten you, but it's not anything that can't be found by doing a quick PubMed search. Birth of two chimeric genes in the Hominidae lineage.

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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.

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Accelerated Protein Evolution and Origins of Human-Specific Features. Foxp2 as an example.

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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.

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The Tre2 (USP6) oncogene is a hominoid-specific gene.

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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.

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_____________These are just a few examples of unique genes within human beings (many more will be found when Pan gets sequenced). 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?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.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. 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.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. 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.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.[This message has been edited by Grape Ape, 03-20-2003]

At the DNA and protein level we are 99% plus identical with our primate relatives such as the chimp and the gorilla. What is obvious about our relationship is the fact that the same chromosomal structures have been rearranged. I propose that those position effects are the primary if not sole reasons for our genetic and of course phenotypic differences. Position effects can apparently produce profound differences in the expression of otherwise identical genetic systems, just as Goldschmidt postulated in 1940. I refer you to the karyotypes which are pictured in the Manifesto. Of course regulatory genes might also be involved. salty

Sure you can. Maybe the information was already present and simply repressed as it so obviously is in ontogeny. That is basically the crux of my ontogeny paper. salty

Like I said you, have no clear evidence that the changes in the chromosome structure are responsible for major phenotypic changes.Apparently nobody knows if the positional chnages have a significant effect on phenotype or not, while we know that changes to regulatory genes can have major phenotypic effects.

Um, repressed to the point of nonexistence? The examples I pointed out simply do not exist in non-human apes. We're not talking about a case of a "turned-off" gene or anything like that. We're talking about a gene in Homo that is coding and functional versus the complete absence of any such gene in Pan or other great apes. And it's not as if we don't know how these new genes evolve.Salty, I don't think anyone doubts that chromosomal rearrangements can cause some phenotypic change (other than lethality). But to claim that they are the only method of phenotypic change, you would have to ignore the plethora of site-directed mutagenesis experiments, knock-out experiments, directed protein evolution, and observed instances of selection both in the lab and in the wild. In short, you'd have to ignore nearly everything we know about molecular evolution. Furthermore, how do you establish that the rearrangements that we've had are anywhere close to sufficient? The karyotypes between humans and chimps are highly similar. The biggest difference is the Robersonian fusion of chromosome 2. And I believe that there are a few arm translocations. But it ain't much. The fossil record shows that we've gone through quite a few intermediate stages since our divergence from Pan. How do account for that with a handful of rearrangements?

Yes, you were, but you assigned this to Darwinians as the foundation of their acceptance of gradual genetic change: Not only is this *not* the position of Darwinians, it doesn't even make sense since rate of occurrence of events and the duration of individual events are two different things.I'm sure you agree that it makes no sense to assign your opponents positions they do not hold, and that you want to make your position as solid as possible by correcting and/or removing confusions or mistakes. Since Moose entered your first post for you you cannot edit it (you can always edit your own posts), so let me know if it's alright if I modify it for you.------------------
--EvC Forum Administrator

It is the height of arrogance to suggest that anyone edit another persons posts. I stand on what I have said thank you. Let me suggest that rearrangement of chromosomes can result in the release of genes that were there all along. There is a huge amount of DNA that is not doing anything. Could that not represent the potential stockpile that evolving organisms have tapped into during their evolutionary appearance and ultimate fixation? Why must one always postulate mutation and selection to explain every genetic difference that one encounters? I admit that I am not a molecular biologist and so I am not conversant with it all. I simply am reasoning by analogy with development. Let me put it this way. Are new genes involved in the differentiation of the adult from the fertilized egg? Are not the genes already present at the beginning of ontogeny? All I have postulated is that the same might be true during evolution. DeHaan seems to think this has merit. I also don't see anything wrong with being an advocate of intelligent design. Frankly, I don't see how anyone can deny it. The idea that evolution involved the unfolding of preexisting information is very old. It was proposed by Bateson and later by Leo Berg who called it phylogenetic acceleration when advanced features appeared in primitive organisms In any event I see no compelling evidence that either chance or selection had anything to do with macroevolution (speciation). I realize it is difficult to understand how either ontogeny or phylogeny can occur. They are both enormous mysteries.