Cdk1, but not Cdk2, is the sole Cdk that is essential and sufficient to drive resumption of meiosis in mouse oocytes

Research output: Contribution to journalArticle

Abstract

Mammalian oocytes are arrested at the prophase of meiosis I during fetal or postnatal development, and the meiosis is resumed by the preovulatory surge of luteinizing hormone. The in vivo functional roles of cyclin-dependent kinases (Cdks) during the resumption of meiosis in mammalian oocytes are largely unknown. Previous studies have shown that deletions of Cdk3, Cdk4 or Cdk6 in mice result in viable animals with normal oocyte maturation, indicating that these Cdks are not essential for the meiotic maturation of oocytes. In addition, conventional knockout of Cdk1 and Cdk2 leads to embryonic lethality and postnatal follicular depletion, respectively, making it impossible to study the functions of Cdk1 and Cdk2 in oocyte meiosis. In this study, we generated conditional knockout mice with oocyte-specific deletions of Cdk1 and Cdk2. We showed that the lack of Cdk1, but not of Cdk2, leads to female infertility due to a failure of the resumption of meiosis in the oocyte. Re-introduction of Cdk1 mRNA into Cdk1-null oocytes largely resumed meiosis. Thus, Cdk1 is the sole Cdk that is essential and sufficient to drive resumption of meiosis in mouse oocytes. We also found that Cdk1 maintains the phosphorylation status of protein phosphatase 1 and lamin A/C in oocytes in order for meiosis resumption to occur.

Details

Authors
  • Deepak Adhikari
  • Wenjing Zheng
  • Yan Shen
  • Nagaraju Gorre
  • Yao Ning
  • Guillaume Halet
  • Philipp Kaldis
  • Kui Liu
External organisations
  • University of Gothenburg
  • Umeå University
  • National University of Singapore
Original languageEnglish
Article numberdds061
Pages (from-to)2476-2484
JournalHuman Molecular Genetics
Volume21
Issue number11
Publication statusPublished - 2012 Jun 1
Publication categoryResearch
Peer-reviewedYes
Externally publishedYes