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Development. 2019 Apr 26;146(8). pii: dev172734. doi: 10.1242/dev.172734.

Cyclin B2 is required for progression through meiosis in mouse oocytes.

Daldello EM1,2,3, Luong XG1,2,3, Yang CR1,2,3, Kuhn J4, Conti M5,2,3.

Author information

1
Center for Reproductive Sciences, University of California, San Francisco, CA 94143, USA.
2
Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco, CA 94143, USA.
3
Department of Obstetrics and Gynecology and Reproductive Sciences, University of California, San Francisco, CA 94143, USA.
4
Cell and Tissue Biology Department, University of California, San Francisco, CA 94143, USA.
5
Center for Reproductive Sciences, University of California, San Francisco, CA 94143, USA contim@obgyn.ucsf.edu.

Abstract

Cyclins associate with cyclin-dependent serine/threonine kinase 1 (CDK1) to generate the M phase-promoting factor (MPF) activity essential for progression through mitosis and meiosis. Although cyclin B1 (CCNB1) is required for embryo development, previous studies concluded that CCNB2 is dispensable for cell cycle progression. Given previous findings of high Ccnb2 mRNA translation rates in prophase-arrested oocytes, we re-evaluated the role of this cyclin during meiosis. Ccnb2 -/- oocytes underwent delayed germinal vesicle breakdown and showed defects during the metaphase-to-anaphase transition. This defective maturation was associated with compromised Ccnb1 and Moloney sarcoma oncogene (Mos) mRNA translation, delayed spindle assembly and increased errors in chromosome segregation. Given these defects, a significant percentage of oocytes failed to complete meiosis I because the spindle assembly checkpoint remained active and anaphase-promoting complex/cyclosome function was inhibited. In vivo, CCNB2 depletion caused ovulation of immature oocytes, premature ovarian failure, and compromised female fecundity. These findings demonstrate that CCNB2 is required to assemble sufficient pre-MPF for timely meiosis re-entry and progression. Although endogenous cyclins cannot compensate, overexpression of CCNB1/2 rescues the meiotic phenotypes, indicating similar molecular properties but divergent modes of regulation of these cyclins.

KEYWORDS:

Cyclins; Fertility; MPF; Meiosis; Mouse oocytes

PMID:
30952665
PMCID:
PMC6503990
[Available on 2020-04-15]
DOI:
10.1242/dev.172734

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