The spindle assembly checkpoint is not essential for CSF arrest of mouse oocytes

Chizuko Tsurumi1, Steffen Hoffmann, Stephan Geley

  • 1Max-Planck-Institut fuer Immunbiologie, Developmental Biology, Freiburg, Germany. tsurumi@immunbio.mpg.de

The Journal of Cell Biology
|December 22, 2004
PubMed

Insights

Mouse oocytes utilize spindle assembly checkpoint (SAC) proteins for meiosis I and II checkpoints. However, unlike frog eggs, the SAC is not essential for maintaining metaphase arrest in mouse oocytes.

Area of Science:

  • Cell biology
  • Developmental biology
  • Reproductive biology

Background:

  • The spindle assembly checkpoint (SAC) is crucial for accurate chromosome segregation.
  • Bub1 kinase plays a known role in SAC function during meiosis II arrest in Xenopus oocytes.

Purpose of the Study:

  • To determine if SAC-mediated inhibition of the anaphase-promoting complex/cyclosome (APC/C) maintains metaphase arrest in mouse oocytes.
  • To investigate the role of SAC proteins in cytostatic factor (CSF)-induced arrest.

Main Methods:

  • Injection of dominant-negative Bub1 mutant (Bub1dn) into mouse oocytes.
  • In vitro meiosis progression analysis.
  • Assessment of metaphase II arrest following CSF release and nocodazole treatment.

Main Results:

  • Disruption of SAC by Bub1dn accelerated meiosis I passage but did not prevent metaphase II arrest.
  • Bub1dn-injected oocytes entered interphase upon CSF release and spindle disruption, unlike controls.
  • Similar results observed with dominant-negative Mad2, BubR1, and APC/C-activating Cdc20 mutants.

Conclusions:

  • SAC proteins are required for checkpoint functions in both meiosis I and II in mouse oocytes.
  • The SAC is not required for establishing or maintaining CSF arrest in mouse oocytes, contrasting with findings in frog eggs.

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