Cyclin B1/Cdk1 coordinates mitochondrial respiration for Cell-Cycle G2/M progression

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

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)217-232
Number of pages16
JournalDevelopmental Cell
Volume29
Issue number2
DOIs
StatePublished - Apr 28 2014
Externally publishedYes

ASJC Scopus subject areas

  • Developmental Biology

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