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JMY is required for asymmetric division and cytokinesis in mouse oocytes

Shao-Chen Sun1, Qing-Yuan Sun, Nam-Hyung Kim

  • 1Department of Animal Sciences, Chungbuk National University, Cheongju 361-763, Korea.

Molecular Human Reproduction
|January 27, 2011
PubMed

Insights

JMY protein is crucial for mouse oocyte maturation, regulating spindle migration and asymmetric cell division. Its depletion causes developmental arrest and abnormal cell formation.

Area of Science:

  • Cell Biology
  • Reproductive Biology
  • Molecular Biology

Background:

  • JMY (JAB1/MOV10-like) is a known p53 co-factor and actin nucleation factor in somatic cells.
  • Its function in mouse oocyte meiotic maturation remains uncharacterized.

Purpose of the Study:

  • To investigate the expression and function of JMY during mouse oocyte meiotic maturation.
  • To elucidate JMY's role in key processes like spindle migration, asymmetric division, and cytokinesis.

Main Methods:

  • Quantitative analysis of JMY mRNA expression during oocyte maturation stages.
  • Immunolocalization of JMY protein within oocytes.
  • Functional studies using JMY depletion via RNA interference (RNAi) and antibody injection.

Main Results:

  • JMY mRNA expression peaks from germinal vesicle to metaphase I and declines thereafter.
  • JMY localizes to the spindle and cytoplasm of oocytes.
  • JMY depletion leads to symmetric division, failed spindle migration, cytokinesis failure, and TI stage arrest, resulting in 2-cell-like MII oocytes.
  • Disruption of actin cap and cortical granule-free domain formation indicates impaired spindle migration.

Conclusions:

  • JMY is essential for establishing oocyte polarity.
  • JMY plays a critical role in regulating spindle migration, asymmetric division, and cytokinesis during mouse oocyte meiotic maturation.

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