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Scc1 sumoylation by Mms21 promotes sister chromatid recombination through counteracting Wapl

Nan Wu1, Xiangduo Kong, Zhejian Ji

  • 1Howard Hughes Medical Institute, Department of Pharmacology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

Genes & Development
|July 4, 2012
PubMed

Insights

The Smc5/6 subunit Mms21 sumoylates cohesin, promoting DNA double-strand break repair. This sumoylation is crucial for homologous recombination and prevents sensitivity to DNA damage.

Area of Science:

  • Cellular biology
  • Molecular genetics
  • DNA repair mechanisms

Background:

  • DNA double-strand breaks (DSBs) are critical in cancer development.
  • Sister chromatid homologous recombination (SCR) repairs DSBs.
  • Cohesin and Smc5/6 complexes are vital for DSB repair.

Purpose of the Study:

  • To investigate the role of Mms21-mediated sumoylation of cohesin in DSB repair.
  • To understand how Scc1 sumoylation impacts SCR and genome stability.

Main Methods:

  • Investigated Mms21 sumoylation of the cohesin subunit Scc1.
  • Utilized laser-induced DNA damage in human cells.
  • Assessed SCR efficiency and sensitivity to ionizing radiation (IR).
  • Employed mutants defective in sumoylation and depleted negative cohesin regulators.

Main Results:

  • Mms21 sumoylates Scc1 at multiple lysine residues.
  • Sumoylation is essential for cohesin-dependent SUMO accumulation at DNA damage sites.
  • Cells with non-sumoylatable Scc1 exhibit defects in SCR and increased IR sensitivity.
  • Depletion of Wapl rescues SCR defects in Mms21-deficient or Scc1 mutant cells.

Conclusions:

  • Scc1 sumoylation by Mms21 is a key regulator of SCR.
  • This process antagonizes Wapl, promoting DSB repair post-cohesin loading.
  • The mechanism is independent of Smc3 acetylation, highlighting a distinct regulatory pathway.

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