Loss of PKC mu function induces cytoskeletal defects in mouse oocyte meiosis

Area of Science:

• Cell Biology
• Developmental Biology
• Reproductive Biology

Background:

• The cytoskeleton, comprising microtubule and actin filaments, is vital for mammalian oocyte maturation.
• Protein kinase C mu (PKC mu) has emerged as a potential regulator of cytoskeletal dynamics during this process.

Purpose of the Study:

• To investigate the role of PKC mu in mouse oocyte maturation and its impact on cytoskeletal organization.
• To explore the relationship between PKC mu expression levels and oocyte maturation competence.

Main Methods:

• PKC mu expression and localization were analyzed during oocyte maturation.
• Morpholino injection was used to knockdown PKC mu expression in oocytes.
• Oocyte maturation rates, polar body extrusion, division symmetry, spindle organization, tubulin acetylation, and cofilin phosphorylation were assessed.

Main Results:

• PKC mu was expressed and localized at spindle poles during oocyte maturation, with reduced expression in aged or in vitro cultured oocytes.
• PKC mu knockdown led to decreased oocyte maturation competence, evidenced by reduced polar body extrusion and increased symmetric division.
• Loss of PKC mu resulted in spindle organization defects, indicated by decreased tubulin acetylation.
• PKC mu influenced cofilin phosphorylation, affecting actin assembly, cytoplasmic actin distribution, and spindle positioning.

Conclusions:

• PKC mu is a key factor in mammalian oocyte maturation.
• PKC mu regulates oocyte maturation by maintaining proper spindle organization and controlling actin filament distribution.