Journal
CELL REPORTS
Volume 24, Issue 12, Pages 3262-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.08.047
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Funding
- Spanish Ministry of Economy and Competitivity [SAF2016-74855-P]
- FPU fellowships from the Spanish Ministry of Education
- University of Sevilla (V Plan Propio)
- regional government of Andalucia (Junta de Andalucia)
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DNA breaks are complex lesions that can be repaired either by non-homologous end joining (NHEJ) or by homologous recombination (HR). The decision between these two routes of DNA repair is a key point of the DNA damage response (DDR) that is controlled by DNA resection. The core machinery catalyzing the resection process is well established. However, little is known about the additional requirements of DNA resection over DNA structures with high complexity. Here, we found evidence that the human helicase PIF1 has a role in DNA resection, specifically for defined DNA regions, such as those prone to form G-quadruplexes. Indeed, PIF1 is recruited to the site of DNA damage and physically interacts with proteins involved in DNA resection, and its depletion causes DNA damage sensitivity and a reduction of HR efficiency. Moreover, G4 stabilization by itself hampers DNA resection, a phenomenon suppressed by PIF1 overexpression.
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