Disrupted MOS signaling alters meiotic cell cycle regulation and the egg transcriptome

Area of Science:

• Reproductive biology
• Cellular and molecular biology
• Developmental biology

Background:

• Mammalian female meiosis requires precise regulation for producing a viable egg.
• Oocytes arrest at prophase I until puberty and resume meiosis upon hormonal stimulation, halting new transcription.
• The MOS kinase regulates the metaphase II arrest via the MAPK pathway, essential for egg competency and fertility.

Purpose of the Study:

• To investigate the consequences of MOS kinase deletion on female meiosis.
• To understand MOS's role in coordinating meiotic divisions and maintaining egg transcriptome.

Main Methods:

• Live imaging of mouse oocytes with and without MOS.
• Analysis of meiotic progression and polar body extrusion.
• Single-egg sequencing to assess gene expression profiles.

Main Results:

• Mos-deficient (mos-/-) eggs show transient chromosome separation in meiosis I and abnormal divisions.
• New transcription is required for additional divisions in mos-/- eggs but not for second polar body extrusion.
• Significant differences in gene expression were observed between wildtype and mos-/- eggs, with altered cell cycle regulation, RNA metabolism, and transcription pathways.

Conclusions:

• MOS is critical for meiotic cell cycle regulation and timely meiotic progression.
• MOS ensures the egg maintains a specific transcriptome essential for developmental competence.
• Disruption of MOS function leads to aberrant meiotic events and altered gene expression, affecting fertility.