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Cyclin B1/Cdk1 coordinates mitochondrial respiration for cell-cycle G2/M progression.

Wang Z., Fan M., Candas D., Zhang T.Q., Qin L., Eldridge A., Wachsmann-Hogiu S., Ahmed K.M., Chromy B.A., Nantajit D., Duru N., He F., Chen M., Finkel T., Weinstein L.S., Li J.J.

A substantial amount of mitochondrial energy is required for cell-cycle progression. The mechanisms underlying the coordination of the mitochondrial respiration with cell-cycle progression, especially the G2/M transition, remain to be elucidated. Here, we show that a fraction of cyclin B1/Cdk1 proteins localizes to the matrix of mitochondria and phosphorylates a cluster of mitochondrial proteins, including the complex I (CI) subunits in the respiratory chain. Cyclin B1/Cdk1-mediated CI phosphorylation enhances CI activity, whereas deficiency of such phosphorylation in each of the relevant CI subunits results in impairment of CI function. Mitochondria-targeted cyclin B1/Cdk1 increases mitochondrial respiration with enhanced oxygen consumption and ATP generation, which provides cells with efficient bioenergy for G2/M transition and shortens overall cell-cycle time. Thus, cyclin B1/Cdk1-mediated phosphorylation of mitochondrial substrates allows cells to sense and respond to increased energy demand for G2/M transition and, subsequently, to upregulate mitochondrial respiration for successful cell-cycle progression.

Dev. Cell 29:217-232(2014) [PubMed] [Europe PMC]