Caloric restriction slows brain aging

Paul S. Brookes. brookes at uab.edu
Tue Jul 11 11:31:30 EST 2000


Aubrey,

I think your comment, about inserting hydrophobic proteins into 
mitochondria only being a problem until such time as we can develop 
technology to get around it, raises an intersting point.  Surely if man can 
develop such technology on a short timescale then nature would have done so 
already.  So, given that the "toxicity of redox proteins" doesn't hold much 
water either, then there really must be a very, very, very good reason for 
retaining some proteins in the mtDNA, and I don't think anyone has really 
provided a watertight answer to this yet.

On the side - do the proteins that are mtDNA encoded have significant flux 
control within their respective complexes (versus the nuclear encoded 
ones)? - assuming its possible that flux control exists between the 
individual sub-units of a protein but that's another story.    This brings 
us to the issue of regulation of mitochondrial gene expression in the 
context of control of respiration.   Is it just that these proteins have to 
be on mtDNA so they're readily up/down-regulated in response to 
mitochondria-specific stimuli?   Moving them to the nucleus results in loss 
of this important control mechanism, because the nucleus cannot sense the 
things that might control mito gene expression (such as redox status, 
matrix pH, Ca2+, ATP, whatever).  Thus, merely transporting mtDNA genes to 
the nucleus is only the beginning of the story - and learning how to 
regulate their expression in response to mitochondria-specific stimuli is 
another issue.

Any chance of a tibtech article preprint?
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

The quality of e-mails can go down as well as up
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