We may have answered his question. A little background:
Recently, we noted that prominent science writer Carl Zimmer was in a tangle with Discovery Institute’s David Klinghoffer arising from a discussion on a Facebook page: His issue here was this paragraph:
But the idea of such an event having occurred at all is itself far from sure. The telomeric DNA parked in the middle of chromosome 2 is not a unique phenomenon. Other mammals have it too, across their own genomes. Even if it were unique, there’s much less of it than you would expect from the amalgamation of two telomeres. Finally, it appears in a “degenerate,” “highly diverged” form that should not be the case if the joining happened in the recent past, circa 6 million years ago, as the Darwinian interpretation holds.
I was baffled, so I asked on Facebook for the evidence that the form of the chromosome wasn’t what you’d expect if it fused six million years ago.
What followed was a ridiculous runaround, some of which I’ll reproduce here: More.
Well, a reader writes to say, here is where the idea might have originated:
This 1991 Pub Med paper:
Genomic divergences between humans and other hominoids and the effective population size of the common ancestor of humans and chimpanzees.
Chen FC, Li WH., Department of Life Science, National Tsing Hua University, Taiwan.
If the fusion occurred within the telomeric repeat arrays less than ~6 Mya, why are the arrays at the fusion site so degenerate? The arrays are 14% diverged from canonical telomere repeats (not shown), whereas noncoding sequence has diverged There are three possible explanations: (1) Given the many instances of degenerate telomeric arrays within the subtelomeric regions of human chromosomes (Riethman et al. 2001), the chromosomes joined at interstitial arrays near, but not actually at, their ends. In this case, material from the very ends of the fusion partners would have been discarded. (2) The arrays were originally true terminal arrays that degenerated rapidly after the fusion. This high rate of change is plausible, given the remarkably high allelic variation observed at the fusion site. The arrays in the BAC and the sequence obtained by Ijdo et al. (1991) differ by 12%, which is high even if some differences are ascribed to experimental error. (3) Some array degeneracy could be a consequence of sequencing errors. We have not been able to PCR successfully across the fusion site, which would be required to assess the contribution of sequencing errors to this measure of fusion-site sequence polymorphism. However, explanation 2 is supported by the high variability among allelic copies of other interstitial telomeric repeats and associated regions sequenced by Mondello et al. (2000) (AF236886 and AF236885). Considering the high mutability of interstitial telomere repeat arrays, the fusion partners could have joined either within terminal or subterminal arrays to form chromosome 2.
Was this where the idea originated?
Now Carl Zimmer is free to read the book anyway.
See also: Here, Cornelius Hunter addresses the Zimmer-Klinghoffer conflict.
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