Cyclin B3-CDK1 couples translational de-repression to embryonic mitoses via OMA protein degradation in C. elegans

David Bojorquez1, Shabnam Moghareh1, Maab Elsayed1

  • 1Department of Developmental & Cell Biology, University of California Irvine, Irvine, CA 92697, USA.

Insights

The cyclin B3-CDK1 complex controls early gene expression in C. elegans by degrading RNA-binding proteins, ensuring mRNA translation during embryogenesis. This process couples cell division with developmental gene activation.

Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Cell Biology

Background:

  • Early embryogenesis relies on maternal mRNAs translated under RNA-binding protein control.
  • The cyclin B3-CDK1 complex is known for its role in mitosis.

Purpose of the Study:

  • To investigate the role of the cyclin B3-CDK1 complex in early embryonic gene expression in C. elegans.
  • To elucidate the mechanism by which cyclin B3-CDK1 regulates translation of maternal mRNAs.

Main Methods:

  • Utilized C. elegans model system.
  • Investigated protein degradation pathways.
  • Analyzed RNA binding protein function and mRNA translation.
  • Examined the role of cyclin B3 phosphorylation sites.

Main Results:

  • Identified cyclin B3-CDK1 complex as critical for early embryonic gene expression in C. elegans.
  • Demonstrated that cyclin B3-CDK1 targets RNA binding OMA proteins (OMA-1, OMA-2) for degradation.
  • Showed OMA protein degradation is essential for de-repression and translation of target mRNAs.
  • Discovered that cyclin B3's phosphate-binding pocket is crucial for OMA phosphorylation and degradation, but separable from its mitotic functions.

Conclusions:

  • The cyclin B3-CDK1 complex plays a dual role in early development, regulating both mitotic divisions and mRNA translation.
  • Embryonic activation of cyclin B3-CDK1 couples cell division with the early gene expression program.
  • Separable mitotic and translational functions of cyclin B3-CDK1 highlight distinct regulatory mechanisms.

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