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Tbf1 and Vid22 promote resection and non‐homologous end joining of DNA double‐strand break ends
Author(s) -
Bonetti Diego,
Anbalagan Savani,
Lucchini Giovanna,
Clerici Michela,
Longhese Maria Pia
Publication year - 2013
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2012.327
Subject(s) - biology , non homologous end joining , homologous recombination , dna , genetics , homologous chromosome , computational biology , microbiology and biotechnology , gene
The repair of DNA double‐strand breaks (DSBs) is crucial for maintaining genome stability. The Saccharomyces cerevisiae protein Tbf1, which is characterized by a Myb domain and is related to mammalian TRF1 and TRF2, has been proposed to act as a transcriptional activator. Here, we show that Tbf1 and its interacting protein Vid22 are new players in the response to DSBs. Inactivation of either TBF1 or VID22 causes hypersensitivity to DSB‐inducing agents and shows strong negative interactions with mutations affecting homologous recombination. Furthermore, Tbf1 and Vid22 are recruited to an HO‐induced DSB, where they promote both resection of DNA ends and repair by non‐homologous end joining. Finally, inactivation of either Tbf1 or Vid22 impairs nucleosome eviction around the DSB, suggesting that these proteins promote efficient repair of the break by influencing chromatin identity in its surroundings.