Cyclin B Translation Depends on mTOR Activity after Fertilization in Sea Urchin Embryos

Héloïse Chassé1,2, Odile Mulner-Lorillon1,2, Sandrine Boulben1,2

  • 1Sorbonne Universités, UPMC Univ Paris 06, UMR 8227, Integrative Biology of Marine Models, Translation Cell Cycle and Development, Station Biologique de Roscoff, CS 90074, F-29688, Roscoff cedex, France.

Plos One
|March 11, 2016
PubMed

Insights

The mTOR pathway regulates cyclin B translation after fertilization in sea urchins. This involves inhibiting the repressor 4E-BP (eukaryotic initiation factor 4E-Binding Protein), controlling cell cycle entry.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • The cyclin B/CDK1 complex is crucial for initiating mitosis.
  • The mTOR signaling pathway plays a role in regulating cellular processes.

Purpose of the Study:

  • To investigate the role of the mTOR signaling pathway in controlling cyclin B mRNA translation following fertilization in sea urchin eggs.
  • To elucidate the mechanisms by which mTOR influences cell cycle entry.

Main Methods:

  • Utilized PP242, an ATP-competitive mTOR kinase inhibitor.
  • Assessed global protein synthesis, cyclin B accumulation, and cyclin B/CDK1 complex activation.
  • Analyzed cyclin B mRNA recruitment into active polysomes.

Main Results:

  • PP242 treatment inhibited global protein synthesis and delayed cyclin B accumulation and CDK1 activation.
  • PP242 inhibited cyclin B mRNA recruitment into polysomes, suggesting control over translation.
  • A portion of cyclin B mRNA translation was found to be insensitive to PP242.

Conclusions:

  • The mTOR pathway, via inhibition of 4E-BP (eukaryotic initiation factor 4E-Binding Protein), controls cyclin B mRNA translation post-fertilization in sea urchins.
  • Cyclin B mRNA translation is regulated by both PP242-sensitive (mTOR-dependent) and PP242-insensitive mechanisms.

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