Distinguishing Design from Accidental Events: Part One

Uncommon Descent featured this post which debunks some Talk Origins concepts. Among them is the TO view of tandem repeats. TO is quoted as stating that "scientists view tandem repeat sequences as resulting from accidental DNA duplications.” Then the actual roles of tandem repeats are laid out. They include silencing and activating genes. Tandom repeats are associated with specific promoters. They are linked to the lengths of dog noses and the percentage of fat in cow's milk. Tandom repeats are also believed to be a causal factor in determining the appearance of individuals; traits like amount of body fat, height, skin color and more. In fact, tandom repeats are so individually unique that they function like molecular fingerprints.

Does all this appear to result from "accidental DNA duplications?" If it does and tandem repeats influence such properties as body fat, milk fat, nose length, height, skin color and more then what determined these properties prior to these accidents? If you are familiar with the respective views of intelligent design advocates and the mainstream evolutionary community, then you know that the latter will explain any set of outcomes as consistent with their views. If tandem repeats were found to confer no functional utility then the associated explanation would be "what would you expect of accidental duplications?" If function is found then that too can be explained by random, selected changes. Tails I win, heads I win too.

What does TO have to say about transposons? As quoted by UD:

"In many ways, transposons are very similar to viruses. However, they lack genes for viral coat proteins, cannot cross cellular boundaries, and thus they replicate only in the genome of their host. They can be thought of as intragenomic parasites.…finding the same transposon in the same chromosomal location in two different organisms is strong direct evidence of common ancestry, since they insert fairly randomly and generally cannot be transmitted except by inheritance…."

A good set up argument for common ancestry but there is more to this. Fairly random insertion is dubious as this linked study indicates. "Analysis of in vivo integration patterns has provided no data to support the notion that retroelement integration is random. Rather, the diversity of insertion patterns of retroelements suggests numerous ways in which genomic DNA is identified for preferential targeting."1

And there is this: "Retrotransposon and retroviral insertions are not randomly distributed on chromosomes, suggesting that retroelements actively select integration sites. This is the case for the yeast Ty5 retrotransposons, which preferentially integrate into domains of silent chromatin at the HM loci and telomeres."2



1. PubMed; 'Integration specificity of retrotransposons and retroviruses;' Sandmeyer SB, Hansen LJ, Chalker DL.

2. Genes & Development; Vol. 13, No. 20, pp. 2738-2749, October 15, 1999;
'Tagging chromatin with retrotransposons: target specificity of the Saccharomyces Ty5 retrotransposon changes with the chromosomal localization of Sir3p and Sir4p;'
Yunxia Zhu, Sige Zou, David A. Wright, and Daniel F. Voytas