>>Yeah, finish reading the paper you schmuck

>>

>>LOL! Now, is that any way to talk to someone who could one day be looking at you down the barrel of a hypodermic?

>>



LOL! My humblest regards kind sir



>>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.

>>

>>Very intriguing indeed! This could be evidence of targeted mutation. Recently, a family of proteins was discovered that inflicts deamination upon cytosine in nucleic acids, creating uracil in its place. The presence of uracil in DNA is a problem (but OK in RNA, as you know), so mechanisms are in place to quickly recognize and correct this lesion. In immunoglobulin producing cells, the dC-->dU lesions produced by one of these deaminase proteins are repaired in ways that can produce somatic hypermutation, gene conversion (using nearby pseudogenes as repair templates!), and class-switch recombination. This, except for C-SR, is targeted to genes encoding variable regions on immunoglobulins (the regions that actually contact antigen), apparently by recognizing CG dinucleotide pairs that occur in specific contexts.

>>

>>Since you and Wolfgang have uncovered the existence of high structural diversity within venom toxin families, I would not be surprised if a mutation-targeting mechanism is discovered "dancing among the toxin genes".



Yes, the degree of seemingly targeted hyper-variability is extraordinary we find it extremely interesting.



>Damn fine stuff!



Fangs for that



Cheers

B
-----
Dr. Bryan Grieg Fry

Deputy Director

Australian Venom Research Unit

University of Melbourne



www.venomdoc.com

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