DNA repair

Iuval clejan clejan at mindspring.com
Tue Dec 19 14:11:24 EST 2000


"Dr. Sydney Shall" wrote:

> > 2. Are there any studies of how the nuclear genes coding for mtDNA
> > repair enzymes are themselves repaired? One can imagine a stable
system
> > (biological or cybernetic) in which all repair mechanisms can also
> > repair each other (it's stable because it would take SIMULTANEOUS
damage
> > to all repair mechanisms to destabilize it, which is unlikely), but
if
> > the nodes of this system are not all connected  to each other (i.e.
> > repairing each other) and there is an achiles heel node that is
least
> > connected, the system would become unstable over time and might
exhibit
> > some of the characteristics of ageing. Is pol gamma the only repair
> > enzyme for mtDNA? Does the nuc gene encoding it get repaired by
anything
>
> > else?
> >
>
> This is an interesting point.  Clearly the GENES coding for the repair

> proteins are repaired by these proteins.  This is OK, however because
they
> can stop making proteins temporarily with safety
>

But this is unstable because if a gene codes for its own repair protein,
a
mutation of the gene is likely to either stop coding for anything or
code for
a protein which is ineffectual in repairing. Why can the protein
fabrication be
stopped with safety? If there are other (essential) genes that need to
be
repaired by this protein those genes will be fubared as well, unless
they have
alternative repair proteins. This is really too simplistic. A slightly
more sofisticated system of linear differential equations should answer
some questions about stability
of genes in a web of repair given constant rates of damage/mutation in
both replicating and non-replicating cells. Hypothesis: senescence is
bad for some cells only because for constant rate of mutation, the rate
of repair slows down after senescence and those cells now can't keep up
with the damage. Non replicating cells may have a lower rate of
mutation/damage(?)

-Iuval











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