Aubrey's "survival of the slowest" hypothesis

[Paul S. Brookes.]

Why is it so hard to swallow that ATP availability might not be the only 
signal for mitochondrial proliferation.  In fact, when you think about it, 
it's a pretty poor signal, as mitochondria are not the only things that 
make ATP, and steady state ATP level doesn't really change that much, even 
in a dynamic tissue like the heart (Bob Balaban's NMR studies show this 
quite neatly).    Certainly ATP does not change over the orders of 
magnitude that an archetypal cell signal would change over (think of 
calcium, phosphorylation,or caspase activity as examples - at least 10 fold 
changes involved).   I'm unaware of an ATP-sensitive factor that can sense 
1.2-1.3 fold changes in concentration .

As for what the signal is, why does it have to be the cell itself that 
controls mito' number.   Why not imagine mitochondria as the endosymbiont 
bacteria they are, all competing for food, and having autonomous control 
over their own replication - just like bacteria in a culture dish.  The 
cell can only support a certain number of mito's, and certain cells, 
because they supply more substrates and remove more waste products, can 
support a larger population of mito's.  Thus, it is not so much that a 
signal tells mitochondria to replicate, but that mitochondria will 
replicate un-checked if left to do so, and the important signal is the one 
telling them to stop.  Has anyone looked for repressors of mitochondrial 
replication?

Just a few Friday afternoon thoughts
Paul

_________________________________________
Dr. Paul S. Brookes.            (brookes at uab.edu)
UAB Department of Pathology,   G004 Volker Hall
1670 University Blvd., Birmingham AL 35294 USA
Tel (001) 205 934 1915     Fax (001) 205 934 1775
http://peir.path.uab.edu/brookes


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