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

  • Author(s): Wang, Zhaoqing
  • Fan, Ming
  • Candas, Demet
  • Zhang, Tie-Qiao
  • Qin, Lili
  • Eldridge, Angela
  • Wachsmann-Hogiu, Sebastian
  • Ahmed, Kazi M
  • Chromy, Brett A
  • Nantajit, Danupon
  • Duru, Nadire
  • He, Fuchu
  • Chen, Min
  • Finkel, Toren
  • Weinstein, Lee S
  • Li, Jian Jian
  • et al.
Abstract

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.

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