{'fraction_non_alphanumeric': 0.031067961165048542, 'fraction_numerical': 0.005825242718446602, 'mean_word_length': 5.525316455696203, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Cohesin in DNA damage response and double-strand break repair

Abstract Cohesin, a four-subunit ring comprising SMC1, SMC3, RAD21 and SA1/2, tethers sister chromatids by DNA replication-coupled cohesion (RC-cohesion) to guarantee correct chromosome segregation during cell proliferation. Postreplicative cohesion, also called damage-induced cohesion (DI-cohesion), is an emerging critical player in DNA damage response (DDR). In this review, we sum up recent progress on how cohesin regulates the DNA damage checkpoint activation and repair pathway choice, emphasizing postreplicative cohesin loading and DI-cohesion establishment in yeasts and mammals. DI-cohesion and RC-cohesion show distinct features in many aspects. DI-cohesion near or far from the break sites might undergo different regulations and execute different tasks in DDR and DSB repair. Furthermore, some open questions in this field and the significance of this new scenario to our understanding of genome stability maintenance and cohesinopathies are discussed.