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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