niiicholas
Posts: 319
Joined: May 2002
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Bump as this thread is being cited on ISCID:
http://www.iscid.org/ubbcgi....279&p=2
In the "origin of new information in the evolution of humans" category:
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Genetics 2002 Dec;162(4):1825-35
Accelerated Protein Evolution and Origins of Human-Specific Features. Foxp2 as an example.
Zhang J, Webb DM, Podlaha O.
Department of Ecology and Evolutionary Biology, University of Michigan, Ann Arbor, Michigan 48109.
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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Another one for good measure:
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Science 2001 Feb 16;291(5507):1293-7
Birth of two chimeric genes in the Hominidae lineage.
Courseaux A, Nahon JL.
Institut de Pharmacologie Moleculaire et Cellulaire, UMR CNRS 6097, 660 route des Lucioles Sophia Antipolis 06560 Valbonne, France.
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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[added in edit: oh wait, this was discussed in detail by theyeti back on p. 1
Some points that I think IDists in particular tend to neglect:
1) These are not rare cases, rather discoveries like those referenced here happen every day. The origin of novel genes with divergent functions via natural processes is a ubiquitous and continuing occurrence.
2) I think it is useful to point out how the reconstructed origins of these various genes are *not* due to some single-step process -- rather, we have alternating rounds of duplication, mutation (and *way more* than just point mutation, e.g. exon shuffling) and selection. IDists will often say something like "gene duplication does not create new information because you just have a copy of the gene". But no biologist invokes gene duplication alone. Why don't IDists ever address the case of a gene duplication where one of the copies is mutated and selected, resulting in (1) the original gene and (2) a modified copy with different function. How can the progression of one gene-->two genes with distinct useful functions *not* be an increase in genetic "information" in any biologically relevant sense?
3) If the process described in step 2 is accepted, repeat in a few billion organisms for a few billion years. Does this not go at least a fair distance in explaining the information content of genomes?
4) If the leader of the ID movement, Phil Johnson, is horribly, blatantly wrong about simple biological facts, why has he not been criticized by other IDists? Are they perhaps similarly mislead?
Nick
Edited by niiicholas on Feb. 17 2003,19:27
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