On October 17, 2017, Dr. Huang’s research group published a research article entitled “AUNIP/C1orf135 directs DNA double-strand breaks towards the homologous recombination repair pathway” in Nature Communications.

DNA double-strand breaks (DSBs) are mainly repaired by either homologous recombination (HR) or nonhomologous end-joining (NHEJ). Here we identify AUNIP/C1orf135, a largely uncharacterized protein, as a key determinant of DSB repair pathway choice. AUNIP physically interacts with CtIP and is required for efficient CtIP accumulation at DSBs. AUNIP possesses intrinsic DNA binding ability with a strong preference for DNA substrates that mimic structures generated at stalled replication forks. This ability to bind DNA is necessary for the recruitment of AUNIP and its binding partner CtIP to DSBs, which in turn drives CtIP-dependent DNA-end resection and HR repair. Accordingly, loss of AUNIP or ablation of its ability to bind to DNA results in cell hypersensitivity towards a variety of DSB-inducing agents, particularly those that induce replication-associated DSBs. Our findings provide new insights into the molecular mechanism by which DSBs are recognized and channeled into the HR repair pathway.

Figure：AUNIP directs replication-associated DSB into HR repair

Link:https://www.nature.com/articles/s41467-017-01151-w