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Multiple roles of the splicing complex SF3B in DNA end resection and homologous recombination

AutorPrados-Carvajal, Rosario; López-Saavedra, Ana ; Cepeda-García, Cristina ; Jimeno, Sonia ; Huertas Sánchez, Pablo
Palabras claveDNA resection
CtIP
SF3B
RNA splicing
Homologous recombination
Fecha de publicación2018
EditorElsevier
CitaciónDNA Repair 66-67: 11-23 (2018)
ResumenThe appropriate repair of DNA double strand breaks is critical for genome maintenance. Thus, several cellular pathways collaborate to orchestrate a coordinated response. These include the repair of the breaks, which could be achieved by different mechanisms. A key protein involved in the regulation of the repair of broken chromosomes is CtIP. Here, we have found new partners of CtIP involved in the regulation of DNA break repair through affecting DNA end resection. We focus on the splicing complex SF3B and show that its depletion impairs DNA end resection and hampers homologous recombination. Functionally, SF3B controls CtIP function at, as least, two levels: by affecting CtIP mRNA levels and controlling CtIP recruitment to DNA breaks, in a way that requires ATM-mediated phosphorylation of SF3B2 at serine 289. Indeed, overexpression of CtIP rescues the resection defect caused by SF3B downregulation. Strikingly, other SF3B depletion phenotypes, such as impaired homologous recombination or cellular sensitivity to DNA damaging agents, are independent of CtIP levels, suggesting a more general role of SF3B in controlling the response to chromosome breaks.
URIhttp://hdl.handle.net/10261/165748
Identificadoresdoi: 10.1016/j.dnarep.2018.04.003
e-issn: 1568-7856
issn: 1568-7864
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