Posted by:
BGF
at Sat Oct 11 15:11:07 2003 [ Email Message ] [ Show All Posts by BGF ]
G'day mate
Yeah, finish reading the paper you schmuck 
>ut I was also wondering if mutations in toxin genes seem to occur more frequently or in a non-random manner in exons coding for surface regions whose residues actually contact the target? If so, could this represent evidence that these sequences are intentionally mucked with to generate diversity?
Thats a good question. It seems that mutations happen in pretty much any part of the molecule but that the cysteines and residues flanking them (which could also be considered structural residues and like the cysteines be essential for proper folding of the protein) are highly conserved. However, whether they are conserved through genetic protection (which would require some sort of stencil protein) or alternately when the proteins are produced in the rough endoplasmic reticulum of the cell, misfolded proteins are more sensitive to degradation by housekeeping proteases. The latter scenario is the most likely since it fits with what we already known about cell biology and is also the simplest scenario (which is also a good measure of plausibility). Protection by stencil proteins would be an extraordinarily complex system and also one that has not been discovered.
What is curious though is that the introns consistently undergo less mutation than the exons. This to me seems curious since it would require some sort of way of discriminating between the two at the DNA level. Very intriguing.
Cheers
B
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RE: Elapid venom paper - BGF, Sat Oct 11 15:11:07 2003