An emerging regulatory network of NHEJ via DYNLL1-mediated 53BP1 redistribution

Our bodies are continuously exposed to a wide range of carcinogens and other DNA-damaging agents, together with endogenous forms of DNA damage, resulting in mutations and complex chromosomal aberrations that can affect oncogenes or tumour suppressor genes. These errors, which can be inherited by daughter cells if they are not resolved, can contribute to malignant transformation (1). In tumours, the gradual acquisition of genetic aberrations can also contribute to the development of drug resistance. Various mechanisms that mediate the repair of DNA lesions are critical in suppressing genome instability, thus elucidating these processes is crucial to our understanding of tumour biology and cancer evolution.