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Neddylation inhibits CtIP-mediated resection and regulates DNA double strand break repair pathway choice

Sonia Jimeno1, María Jesús Fernández-Ávila2, Andrés Cruz-García1

  • 1Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), 41092 Sevilla, Spain Departamento de Genética, Universidad de Sevilla, 41080 Sevilla, Spain.

Nucleic Acids Research
|January 9, 2015
PubMed

Insights

Protein neddylation controls DNA repair pathway choice. Inhibiting neddylation boosts homologous recombination, impacting DNA break responses and cell survival.

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA double-strand breaks (DSBs) are highly toxic DNA lesions.
  • Efficient cellular survival depends on precise regulation of DSB repair pathways.

Purpose of the Study:

  • To investigate the role of protein neddylation in controlling DNA repair pathway choice.
  • To elucidate how neddylation influences homologous recombination and non-homologous end joining.

Main Methods:

  • Investigated the effect of neddylation inhibition on DNA repair profiles.
  • Examined the inhibitory role of RNF111/UBE2M-mediated neddylation on DNA end resection.
  • Analyzed the impact of neddylation on single-stranded DNA (ssDNA) length during resection.

Main Results:

  • Protein deneddylation emerges as a key regulator of DNA repair pathway selection.
  • Inhibition of neddylation shifts the repair profile towards increased homologous recombination.
  • RNF111/UBE2M-mediated neddylation inhibits BRCA1 and CtIP-mediated DNA end resection.
  • Neddylation controls ssDNA length, influencing the choice between NHEJ and homologous recombination, and subpathway balance.

Conclusions:

  • Protein neddylation status significantly impacts cellular responses to DNA breaks.
  • Targeting protein neddylation offers a potential strategy to modulate DNA repair pathways.

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