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.

Bonetti, D., Anbalagan, S., Lucchini, G., Clerici, M., & Longhese, M. (2013). Tbf1 and Vid22 promote resection and non-homologous end joining of DNA double-strand break ends. EMBO JOURNAL, 32(2), 275-289 [10.1038/emboj.2012.327].

Tbf1 and Vid22 promote resection and non-homologous end joining of DNA double-strand break ends.

BONETTI, DIEGO
Primo
;
ANBALAGAN, SAVANI;LUCCHINI, GIOVANNA;CLERICI, MICHELA
Penultimo
;
LONGHESE, MARIA PIA
2013

Abstract

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.
Articolo in rivista - Articolo scientifico
Scientifica
chromatin; DSB; NHEJ; resection; Tbf1; Vid22
English
Bonetti, D., Anbalagan, S., Lucchini, G., Clerici, M., & Longhese, M. (2013). Tbf1 and Vid22 promote resection and non-homologous end joining of DNA double-strand break ends. EMBO JOURNAL, 32(2), 275-289 [10.1038/emboj.2012.327].
Bonetti, D; Anbalagan, S; Lucchini, G; Clerici, M; Longhese, M
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/10281/40234
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