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Aberrant cortex contractions impact mammalian oocyte quality.

Elvira Nikalayevich1, Gaëlle Letort2, Ghislain de Labbey1

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Mouse oocytes lacking the Arp2/3 complex exhibit unprecedented cortical contractions, impairing cytoplasmic organization and female fertility. Diminishing these contractions rescues anomalies, suggesting implications for oocyte quality.

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Area of Science:

  • Cell Biology
  • Reproductive Biology
  • Biophysics

Background:

  • The oocyte cortex plays a crucial role in cell shape and chromosome segregation.
  • Actin remodeling in the cortex is essential for proper oocyte function.
  • The Arp2/3 complex is known to regulate cortical actin dynamics.

Purpose of the Study:

  • To investigate the consequences of Arp2/3 complex absence on mouse oocyte cortical remodeling and function.
  • To explore the impact of novel cortical contractions on cytoplasmic organization and female fertility.
  • To examine the presence and implications of similar contractions in human oocytes.

Main Methods:

  • Genetic manipulation to create Arp2/3 complex-deficient mouse oocytes.
  • Advanced imaging techniques to visualize cortical actin dynamics and cytoplasmic activity.
  • Machine learning approaches to analyze cellular contractions and their effects.
  • In vitro fertilization (IVF) procedures for human oocyte collection and analysis.

Main Results:

  • Oocytes lacking the Arp2/3 complex display cortical actin remodeling and unprecedented cortical contractions during division.
  • These contractions lead to cytoplasmic stirring, disrupting organelle organization and activity.
  • Impaired polyspermy prevention capacity reduces female fertility in affected mice.
  • Similar contractions observed in human oocytes correlate with increased cytoplasmic motion but not spindle defects or aneuploidy.

Conclusions:

  • Cortical F-actin dynamics and contractions exert multiscale effects on oocyte cytoplasmic organization.
  • Uncontrolled cortical contractions negatively impact oocyte quality and female fertility.
  • Findings reveal a conserved mechanism in mammalian oocytes with potential implications for IVF and reproductive health.