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The EMSY threonine 207 phospho-site is required for EMSYdriven suppression of DNA damage repair

Petar Jelinic1, Laura A Eccles2, Jill Tseng3

  • 1Laura and Isaac Perlmutter Cancer Center, Division of Gynecologic Oncology, Department of OB/GYN, NYU Langone Medical Center, New York, USA.

Oncotarget
|January 19, 2017
PubMed

Insights

The study reveals that EMSY protein overexpression hinders DNA damage repair, identifying it as a BRCAness gene. This finding suggests EMSY amplification may benefit patients eligible for targeted therapies used in BRCA1/2-mutant cancers.

Area of Science:

  • Genetics and Molecular Biology
  • Cancer Research
  • DNA Repair Mechanisms

Background:

  • BRCA1 and BRCA2 genes are crucial for repairing double-strand DNA breaks, and their alterations are common in breast and ovarian cancers.
  • The gene EMSY is a potential BRCAness gene, and its amplification might impair DNA repair by affecting BRCA2 function.

Purpose of the Study:

  • To investigate the role of EMSY in DNA damage repair.
  • To determine if EMSY belongs to the family of BRCAness proteins.
  • To identify mechanisms underlying EMSY's effect on DNA repair and its potential therapeutic implications.

Main Methods:

  • Direct repeat GFP (DR-GFP) assay to assess DNA repair efficiency.
  • RAD51 foci formation assay to evaluate DNA repair activity.
  • In vitro kinase assays and immunoprecipitation to study protein interactions and phosphorylation.

Main Results:

  • EMSY overexpression was shown to impair DNA damage repair, supporting its classification as a BRCAness protein.
  • A novel phosphorylation site (T207) on EMSY was identified, crucial for its DNA repair suppression activity.
  • Protein kinase A (PKA) was found to directly phosphorylate EMSY at T207.
  • EMSY-mediated DNA repair suppression was demonstrated to be independent of BRCA2 function.
  • EMSY amplification is suggested to be a BRCAness feature.

Conclusions:

  • EMSY plays a significant role in DNA damage repair suppression and is classified as a BRCAness protein.
  • The phosphorylation of EMSY at T207 by PKA is a key mechanism in its function.
  • EMSY amplification may identify a broader patient population for targeted therapies similar to those used for BRCA1/2-mutant cancers.
Keywords:
BRCA2BRCAnessDNA repairEMSYPKA

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