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The mechanism of CSF arrest in vertebrate oocytes

James L Maller1, Markus S Schwab, Stefan D Gross

  • 1The Howard Hughes Medical Institute and Department of Pharmacology, University of Colorado School of Medicine, 4200 E. 9th Avenue, Box C236, Denver, CO 80262, USA. jim.maller@uchsc.edu

Insights

Cytostatic factor (CSF) in Xenopus oocytes arrests meiosis II. This arrest is mediated by Mos and MAPK pathway activation, leading to p90(Rsk) phosphorylating Bub1, which inhibits the anaphase-promoting complex (APC).

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • A cytoplasmic activity, cytostatic factor (CSF), causes metaphase arrest in mature oocytes.
  • In Xenopus, CSF is initiated by progesterone, leading to Mos synthesis and MAPK pathway activation.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying CSF-mediated metaphase arrest in Xenopus oocytes.
  • To identify the downstream targets of the MAPK pathway involved in cell cycle arrest.

Main Methods:

  • Investigated the role of Mos and the MAPK pathway in oocyte maturation.
  • Identified and characterized the function of p90(Rsk) as a key MAPK target.
  • Examined the interaction between p90(Rsk) and Bub1 protein kinase.

Main Results:

  • CSF arrest is dependent on Mos and MAPK pathway activation.
  • p90(Rsk) was identified as the sole MAPK target mediating CSF arrest.
  • p90(Rsk) phosphorylates and activates Bub1, linking the MAPK pathway to the spindle assembly checkpoint.

Conclusions:

  • p90(Rsk) is a crucial mediator of CSF arrest in Xenopus oocytes.
  • The findings establish a link between the MAPK pathway and the spindle assembly checkpoint via Bub1.
  • This mechanism of metaphase arrest is conserved across vertebrates.

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