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Opposing post-translational modifications regulate Cep76 function to suppress centriole amplification.

M Barbelanne1,2, A Chiu1, J Qian1

  • 1Cell Division and Centrosome Biology Research Unit, Institut de Recherches Cliniques de Montréal, Montréal, Québec, Canada.

Oncogene
|April 12, 2016
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Summary
This summary is machine-generated.

Centrosomal protein 76 (Cep76) phosphorylation by CDK2 suppresses centriole amplification. A cancer mutation in Cep76 impairs this suppression, highlighting its role in preventing uncontrolled cell growth.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Biology

Background:

  • Centrioles are essential for cell division and cilia formation.
  • Aberrant centriole copy number is a hallmark of cancer.
  • Mechanisms controlling centriole amplification are not fully understood.

Purpose of the Study:

  • To investigate the role of centrosomal protein 76 (Cep76) in regulating centriole duplication.
  • To elucidate the molecular mechanisms by which Cep76 suppresses centriole amplification.
  • To explore the impact of post-translational modifications on Cep76 function.

Main Methods:

  • Co-immunoprecipitation to study Cep76-CDK2 interaction.
  • Site-directed mutagenesis to analyze Cep76 phosphorylation at S83.
  • Analysis of centriole number in cells expressing wild-type, mutant, or acetylated Cep76.
  • Western blotting to detect phosphorylation and acetylation levels.

Main Results:

  • Cep76 interacts with and is phosphorylated by cyclin A/CDK2 at S83, which suppresses centriole amplification in S phase.
  • A cancer-associated Cep76 mutation (S83C) abrogates this suppressive function.
  • Phosphorylation of Cep76 inhibits polo-like kinase 1 (Plk1) activation, preventing premature centriole disengagement.
  • Acetylation of Cep76 at K279 in G2 phase reduces its inhibitory capacity and precludes S83 phosphorylation.

Conclusions:

  • Temporal regulation of Cep76 post-translational modifications (phosphorylation and acetylation) controls its ability to suppress centriole amplification.
  • Dysregulation of Cep76 function through altered modifications may contribute to cancer development.
  • Cep76 acts as a critical checkpoint for maintaining proper centriole copy number.