Nucleic acids research · 2026
XPA lactylation is required for UV-induced DNA damage repair.
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Yang Jie, Ding Xin, Zeng Zhikai, Yin Hui, He Yiming, Jin Mingpeng, Huang Bingsong, Wang Zhe, Yang Xiaoning, Li Rui, Wang Qianwen, Zhou Xuan, Song Yifei, Li Yu, Wang Xuanhe, Zheng Wen, Lu Lu, Zhu Qian, Liu Jiaqi, Kang Zhihua, Li Lei, Li Yunhui, Wang Chengyuan, Yuan Jian, Chen Yuping, Wu Jinhuan, Yu Bentong
Аннотация
Xeroderma pigmentosum group A (XPA) serves as a core nucleotide excision repair (NER) factor essential for the repair process triggered by UV irradiation. Lactylation, a newly identified post-translational modification, plays a key role in tumorigenesis and cancer progression. Herein, we discovered that XPA was lactylated in the DNA-binding domain by the acyl-transferase KAT5. In addition, UV irradiation promoted XPA lactylation, thereby increasing the chromatin recruitment of XPA and NER. However, the mutation of XPA to a lactylation-deficient form impeded XPA chromatin recruitment under UV irradiation, impaired NER, and rendered cancer cells hypersensitive to UV irradiation. Our data demonstrate that the lactylation of XPA plays a crucial role in NER and reveals the link between metabolic reprogramming and DNA damage repair induced by UV irradiation.