Journal Article

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

Sonia Jimeno, María Jesús Fernández-Ávila, Andrés Cruz-García, Cristina Cepeda-García, Daniel Gómez-Cabello and Pablo Huertas

in Nucleic Acids Research

Volume 43, issue 2, pages 987-999
Published in print January 2015 | ISSN: 0305-1048
Published online January 2015 | e-ISSN: 1362-4962 | DOI: https://dx.doi.org/10.1093/nar/gku1384

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DNA double strand breaks are the most cytotoxic lesions that can occur on the DNA. They can be repaired by different mechanisms and optimal survival requires a tight control between them. Here we uncover protein deneddylation as a major controller of repair pathway choice. Neddylation inhibition changes the normal repair profile toward an increase on homologous recombination. Indeed, RNF111/UBE2M-mediated neddylation acts as an inhibitor of BRCA1 and CtIP-mediated DNA end resection, a key process in repair pathway choice. By controlling the length of ssDNA produced during DNA resection, protein neddylation not only affects the choice between NHEJ and homologous recombination but also controls the balance between different recombination subpathways. Thus, protein neddylation status has a great impact in the way cells respond to DNA breaks.

Journal Article.  8831 words.  Illustrated.

Subjects: Chemistry ; Biochemistry ; Bioinformatics and Computational Biology ; Genetics and Genomics ; Molecular and Cell Biology

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