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However, the mechanisms by which cells rapidly respond to such DNA damage remain largely unknown. In this study, we found that heat shock factor 1 (HSF1), the major transcription factor in the heat shock response, activated several non-homologous end joining (NHEJ) pathway-associated genes, particularly NHEJ1, through puncta formation, thereby maintaining the stability of NHEJ pathway and alleviating the repair burden of DNA double-strand breaks caused by heat stress. Furthermore, N6-methyladenosine (m6A) RNA modification and its reader YTH domain-containing protein 1 (YTHDC1) contributed to this process by promoting the splicing of NHEJ1. Knockdown of HSF1 or YTHDC1 increased nuclear intensity of phosphorylation of histone variant H2AX at Ser-139 (\u03b3H2AX) in heat-stressed cells, whereas NHEJ1 overexpression rescued this effect. Moreover, HSF1 or YTHDC1 overexpression increased NHEJ repair efficiency in heat-stressed cells, supporting the existence of an HSF1\/YTHDC1\u2013NHEJ1\u2013DNA double-strand repair axis. Our findings reveal a mechanism by which cells repair DNA damage during the heat shock response, providing new insights into how cells maintain genomic stability under external stress conditions.<\/jats:p>","DOI":"10.1093\/nar\/gkag418","type":"journal-article","created":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T11:45:56Z","timestamp":1777031156000},"source":"Crossref","is-referenced-by-count":1,"title":["HSF1 and YTHDC1 enhance DNA repair under heat stress by promoting repair-associated gene expression"],"prefix":"10.1093","volume":"54","author":[{"given":"Wenqing","family":"Ding","sequence":"first","affiliation":[{"name":"State Key Laboratory of Gene Function and Modulation Research, School of Life Sciences, Peking-Tsinghua Center for Life Sciences, Beijing Advanced Center of RNA Biology (BEACON), Peking University , Beijing 100871 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