The Saccharomyces cerevisiae 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. Tbf1 localizes at some promoters together with its interacting protein Vid22 and promotes the formation of nucleosome-free regions, suggesting a role for Tbf1 in modulating chromatin organization. As several proteins regulating chromatin dynamics are involved in the DNA damage response (DDR), we explored a possible function of Tbf1 and Vid22 in the DDR. Double-strand breaks (DSBs) are the most harmful DNA damage. DSBs can be repaired by non-homologous end joining (NHEJ) or homologous recombination (HR), which is initiated by 5’-3’ resection of the DSB ends. We show that inactivation of either TBF1 or VID22 causes hypersensitivity to DSB-inducing agents and shows negative interactions with mutations affecting HR. Furthermore, Tbf1 and Vid22 are recruited to an HO-induced DSB, where they promote both resection of DNA ends and repair by NHEJ. Finally, inactivation of either Tbf1 or Vid22 impairs nucleosome eviction around the DSB, suggesting that these proteins promote DSB repair by influencing chromatin identity.

Clerici, M., Bonetti, D., Anbalagan, S., Lucchini, G., & Longhese, M. (2013). The General Regulatory Factor Tbf1 and its interacting protein Vid22 promote repair of DNA double-strand breaks. Intervento presentato a: Revisiting the Central Dogma: Emerging New Concepts in Replication, Transcription and Translation, Pavia.

The General Regulatory Factor Tbf1 and its interacting protein Vid22 promote repair of DNA double-strand breaks

CLERICI, MICHELA;BONETTI, DIEGO;ANBALAGAN, SAVANI;LUCCHINI, GIOVANNA;LONGHESE, MARIA PIA
2013-06

Abstract

The Saccharomyces cerevisiae 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. Tbf1 localizes at some promoters together with its interacting protein Vid22 and promotes the formation of nucleosome-free regions, suggesting a role for Tbf1 in modulating chromatin organization. As several proteins regulating chromatin dynamics are involved in the DNA damage response (DDR), we explored a possible function of Tbf1 and Vid22 in the DDR. Double-strand breaks (DSBs) are the most harmful DNA damage. DSBs can be repaired by non-homologous end joining (NHEJ) or homologous recombination (HR), which is initiated by 5’-3’ resection of the DSB ends. We show that inactivation of either TBF1 or VID22 causes hypersensitivity to DSB-inducing agents and shows negative interactions with mutations affecting HR. Furthermore, Tbf1 and Vid22 are recruited to an HO-induced DSB, where they promote both resection of DNA ends and repair by NHEJ. Finally, inactivation of either Tbf1 or Vid22 impairs nucleosome eviction around the DSB, suggesting that these proteins promote DSB repair by influencing chromatin identity.
No
poster
Scientifica
DNA repair, Transcription, Double strand break
English
Revisiting the Central Dogma: Emerging New Concepts in Replication, Transcription and Translation
Clerici, M., Bonetti, D., Anbalagan, S., Lucchini, G., & Longhese, M. (2013). The General Regulatory Factor Tbf1 and its interacting protein Vid22 promote repair of DNA double-strand breaks. Intervento presentato a: Revisiting the Central Dogma: Emerging New Concepts in Replication, Transcription and Translation, Pavia.
Clerici, M; Bonetti, D; Anbalagan, S; Lucchini, G; Longhese, M
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/10281/52242
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