Ron Grunwald grun at acpub.duke.edu
Wed Jun 19 23:00:32 EST 1996

In article <4qa1fg$r5b at nntp3.u.washington.edu>,
mkkuhner at phylo.genetics.washington.edu (Mary K. Kuhner) wrote:

> In article <4q9fn7$p4k at bolivia.it.earthlink.net> MIKE  LAMB
<mikejonlamb at earthlink.net> writes:
> >Here is one intron benefit: Cancer prevention aid.  Introns can take 
> >hits from chemical carcinogens. These hits might otherwise hit and 
> >mutate an exon causing more damage. The more introns there are, the 
> >fewer damaging mutations occur. 
> But non-transcribed spacers between genes would seem to accomplish the
> same effect with much less cost to the cell.  Synthesizing mRNA
> corresponding to an intron, cutting it out, and throwing it away is a
> mildly expensive operation, and it would seem advantageous to replace it
> with something simpler.

There is a fallacy in these arguments, namely that the number of mutagenic
hits PER GENOME is constant. It seems more likely that the number of
mutations per base pair is fairly constant. Therefore adding more "junk"
would not dilute out the critical targets, it would only increase the
number of mutation events. 

This would certainly be the case for replication errors (most common). I
would think it would also be true for mutagens - the hit rate should be
first order with respect to the nucleotide content (bigger target = more

Ron Grunwald 
Department of Botany
grun at acpub.duke.edu                            

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