BACR AstraZeneca Young Scientist Frank Rose Award: HNRNPUL-1 promotes DNA double-strand break end resection


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Grant Stewart1
1University of Birmingham, UK


The cellular genome is under constant attack from a multitude of both intrinsic and extrinsic agents, which may occur directly, such as exposure to ionizing (IR) or ultraviolet radiation (UV), or indirectly through the generation of reactive oxygen species. While the cell has evolved a complex network of repair pathways that are specialised to recognise and respond to different deleterious DNA lesions, many of the proteins involved are capable of functioning in multiple repair processes. DNA double strand breaks (DSBs) are the most deleterious lesion induced by IR and these are repaired predominantly by two pathways: nonhomologous end-joining (NHEJ) and homologous recombination repair (HRR). Single-stranded DNA (ssDNA) generated by DNA end resection at the DSB is the principle factor that stimulates both ATR-dependent cell cycle checkpoint activation and HRR. DNA end-resection is strictly controlled by Cyclin-dependent kinase activity and is mediated by the hMre11/Nbs1/hRad50 (MRN) complex, CtIP, Exo1 and the RECQ helicase, BLM. Despite our understanding of the cellular components governing endresection, the exact mechanistic details remain unclear.


We have identified a new component of the DNA end-resection pathway that functionally regulates the recruitment of BLM.