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mobile introns

Arlin Stoltzfus arlin at is.dal.ca
Tue Nov 11 22:55:33 EST 1997

cok at mole.bio.cam.ac.uk wrote:

> A phenomemon that I can't seem to rationalise is the (relative)
> confinement of mobile self-splicing introns to organelles. I appreciate
> that:

By "relative" confinement perhaps you intend to imply that these introns 
are not absolutely restricted to organelles.  Group I introns are 
sometimes present in nuclear ribosomal RNA genes in protists, most 
famously in Tetrahymena (the Tom Cech intron), but they have never 
been seen in nuclear protein-coding genes.  They are also found 
in eubacterial tRNAs and in some bacteriophage genes.  Group II introns 
are found very rarely in eubacterial genomes and have never been 
seen in nuclear genomes (but fragments of them have been detected).

This doesn't make the question any less interesting.  In fact it 
makes it more interesting because it shows that the dearth of 
self-splicing introns in non-organellar genomes is not due to 
lack of exposure to these introns. 

> - they may have come into eukaryotes with organelles; BUT this hasn't
> stopped loads of other organelle genes moving to the nucleus.

And they may have brought their group II introns with them.  Because 
the splice donor and acceptor sites are very similar, it has been 
suspected that these introns would rapidly degrade _in situ_ into 
spliceosomal introns by loss of self-splicing ability.  I 
believe it was John Rogers who suggested this in 1989. So we wouldn't 
necessarily expect group II introns in nuclear genes to be maintained 
as such for long periods of time. 
> - they may have evolved into spliceosomal introns in the nucleus, as their
> host organism would develop an interest in making damned sure that it
> retained the machinery to splice them effectively out of coding regions.
> BUT I don't see any reason why mobile self-splicing introns couldn't be
> maintained in the longer term in nuclear genomes just as well as they have
> been in many mitochondrial genomes.
> - long-term maintenance of mobile elements in a genome usually requires
> sex, so that elements can spread to unpopulated genomes. BUT this should
> be even less of a barrier for nuclear mobile introns than for organelle
> ones.

I agree completely.  The rarity of group I introns in non-organellar 
genomes is not due to lack of exposure, and for most nuclear genomes, 
it is not due to the lack of opportunities for selfish spread, which 
would be provided by sexual reproduction.

So, we can conclude that the relative barrier is either they cannot 
get established when introduced, or once established, they face some 
sort of negative selection that is not present in organellar genomes. 

My pet idea is that the distribution of self-splicing introns 
is largely due to a barrier to establishment due to polymerase 
sensitivity to highly structured transcripts, which cause polymerase 
pausing, which is often the first step in termination.  Eukaryotes 
use RNA Pol II for mRNA genes, but RNA Pol I & III for structural 
RNA genes.  Eubacteria (E. coli, at least) transcribe rRNA genes 
from a special promoter that signals termination-resistant
Bacteriophage polymerases are an entirely different class of
Organellar RNA polymerases, curiously, are related to phage polymerases. 
Perhaps structured introns tend to be limited to genes that are 
transcribed by structure-resistant polymerases.  Just a thought (but 
at least its an experimentally tractable one). 


Arlin Stoltzfus, Ph.D. (arlin at is.dal.ca)
Department of Biochemistry, Dalhousie University
Halifax, Nova Scotia B3H 4H7 CANADA
phone: 902-494-2968     fax: 902-494-1355

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