The team started out with a mutant, cobB–, that could not grow on low levels of acetate. They found that the acetyl coenzyme A (CoA) synthetase (Acs) that initially derivatizes acetate to form acetyl CoA was inactive because of acetylation of a specific lysine residue of Acs. CobB, the bacterial Sir2, removed this acetylation and thus activated Acs.
The link to energy status and redox comes about through NAD+. A bacterial cell that is low in energy will use...
The Rockefeller University Press
2003
The Rockefeller University Press
2003
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