Mitochondria apparently adjust their DNA inheritance stategies when faced with different metabolic conditions, based on results from Xin Jie Chen, Ronald Butow, and colleagues (UTSW, Dallas, TX). The key to the change is a metabolic protein called aconitase.
When grown in glucose, budding yeast rely on glycolytic fermentation, but on other carbon sources the Krebs cycle and oxidative fermentation kick in. Aconitase, one element in the Krebs cycle, is turned on when glucose is absent.
The Texas team now shows that this induction helps out not only with the Krebs cycle, but also with the inheritance of mitochondrial DNA (mtDNA). Aconitase turned up as a protein associated with mtDNA; its absence resulted in spores lacking mtDNA. The enzymatic activity of aconitase was not required for mtDNA-stabilizing action. Aconitase could, however, subsitute for another mtDNA nucleoid protein, Abf2p, which is thought to package mtDNA under fermentative conditions.
“Cells go to some trouble to ensure inheritance under different conditions,” says Butow. Although Abf2p is required in fermentative conditions, it seems that aconitase is needed under both fermentative and aerobic, oxidative conditions. Aconitase protects cells lacking Abf2p from ethidium bromide hypersensitivity, but its exact function in packaging, and whether that function helps protect mtDNA from oxidative mutation, remains to be determined. 
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