Proteins are constructed from a string of amino acids, and the amino acid sequence is coded in a gene. But how does the cell know which of its many genes to use in synthesizing proteins? Gene regulation is accomplished via a number of complex mechanisms. For instance, methyl groups are used to tag both the DNA as well as the histone proteins about which the DNA is wrapped. You can read more about histones here and here. In addition to such methylation, histones can also vary by tiny differences in their amino acid sequence. Such histone variants serve as yet another type of tag used for gene regulation. Now new research is revealing the profound complexity of this mechanism.Histone variants are not merely static sign posts that influence gene expression. These variants are moved, by other proteins, between different locations in the genome. The new research elucidates the migration patterns of a histone variant during mouse embryonic development. Cells differentiate over time in the growing embryo, and in this process the histone variant migrates to different genomic locations. And the research indicates these movements are orchestrated by three different proteins. As one researcher put it:
Our work shows that the regulation of histone variant localization -- the shape of the so-called epigenetic landscape at different regions of the genome -- is more complex than previously thought.
Or as one writer explained, these findings “hint at an unimagined complexity of the genome.” Nothing in biology makes sense in the light of evolution.
What is the argument here? Histone gene duplication and divergence as design?
ReplyDelete"Histone variants--ancient wrap artists of the epigenome."
http://www.ncbi.nlm.nih.gov/pubmed/20197778
Robertc
ReplyDelete'What is the argument here?'
I believe the argument is 1) Thesis: Darwinism says all life arose from random mutation. 2) It is impossible for random chance to create super complex living systems, 3) Therefore evolution is false. It is a test of the hypothesis of evolution, nothing more.
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I would say the argument is this: As the post implies, we can't even yet accurately explain how observed phenotypes come to be and persist. Then clearly we have no causal theory that can account for the production of phenotypes (and the hypothetical DNA sequences that supposedly produced them) that we've never observed. Which is to say, we don't know macroevolution is possible, because we have no causal theory that predicts the real and hypothetical phenotypes posited, much less in the right sequential order in the posited time-frame. You can of course just say macroevolution MUST be true because of metaphysical premises, and that's what Dr. Hunter has demonstrated many an evolutionist does.
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