Dear Grape Ape,
In response to:
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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.
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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:
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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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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:
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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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PB: Also GUToB rule #3.
GA's example 3: The Tre2 (USP6) oncogene is a hominoid-specific gene.
quote:
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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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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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