Faid
Posts: 1143
Joined: Mar. 2006
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So, I read the AiG site, and I must say it's just precious.
I realized this: The magic "36%" comes from the 47 point substitutions (of 126 overall) that the human gene shares with the guinea pigs.
That's right, just the substitutions. Suprised? I'm not.
Now, they seem to be aware of the concept of point mutation hotspots, but they try to work around it (?) with this piece of blabber:
| Quote | | It has long been known that mutations are quite non-random in occurrence, but the variety and complexity of mutational hotspots has seldom been appreciated. Rogozin et al.36 have recently summarized our current knowledge of experimentally induced mutations. Many nucleotide motifs other than the earlier-discussed CG doublet can serve as mutational hotspots. It is now known that the sequence content tens of bases away from a given motif can influence the degree of its hotspot behaviour. Moreover, the propensity of nucleotide motifs to be mutational hotspots varies from gene to gene and from one region of the genome to another. Moreover, the foregoing considerations do not even touch the higher-level features of gene or chromatin structure as causes of mutational hotspot behaviour.37 The large relative number of parallel mutations in the guinea pig and primate GULO pseudogenes cannot be said to be unprecedented. Experimental evidence has already demonstrated that nucleotide substitutions (as well as indels, for that matter) can, unexpectedly, occur in a very strongly concerted manner.38 |
Can anyone make sense of it? How does all this argue against hotspots in a given gene? It seems like they're copy/pasting various phrases from different sources, trying to look like they're actually arguing about something. Or, if they seriously think the hotspot concept works for them, how do they explain the much larger simillarity of the broken gene among primates? Oh that's right, they don't.
But maybe I'm wrong, I dunno... The main issue is this: They don't say anything about deletions. At all. For AiG, entire deletions corresponding to exons might as well not exist. And that's in spite of the fact they receive prime mention in their source. They mention something about the exons remaining in humans, but not in relation to guinea pigs, and they forget about it afterwards.
Gee, I wonder why:
| Quote | | Since deletions are not likely to occur independently at the same site and are highly unlikely to be “undone” by later mutations, finding the same deletion in two different individuals or two different species is highly suggestive ofcommon ancestry. (This is in agreement with what is observed in “tracing”certain deletion mutations in human pedigrees.) |
Hey Dave, guess who's been lying to you again?
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A look into DAVE HAWKINS' sense of honesty:
"The truth is that ALL mutations REDUCE information"
"...mutations can add information to a genome. And remember, I have never said that this is not possible."
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