interferon and immune responses
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It is found that naked mole-rat cyclic guanosine monophosphate-adenosine monophosphate-adenosine monophosphate synthase (cGAS) lacks the suppressive function of human or mouse homologs in homologous recombination repair through the alteration of four amino acids during evolution, which enables cGAS to retain chromatin longer upon DNA damage.
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Efficient DNA repair might make possible the longevity of naked mole-rats. However, whether they have distinctive mechanisms to optimize functions of DNA repair suppressors is unclear. We find that naked mole-rat cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS) lacks the suppressive function of human or mouse homologs in homologous recombination repair through the alteration of four amino acids during evolution. The changes enable cGAS to retain chromatin longer upon DNA damage by weakening TRIM41-mediated ubiquitination and interaction with the segregase P97. Prolonged chromatin binding of cGAS enhanced the interaction between repair factors FANCI and RAD50 to facilitate RAD50 recruitment to damage sites, thereby potentiating homologous recombination repair. Moreover, the four amino acids mediate the function of cGAS in antagonizing cellular and tissue aging and extending life span. Manipulating cGAS might therefore constitute a mechanism for life-span extension.
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@article{Chen2025cGAS,
title = {A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging},
author = {Yu Chen and Z Q Chen and Hao Wang and Zhen Cui and Kaile Li and Zhiwei Song and Lingjiang Chen and Xiaoxiang Sun and Xiaoyu Xu and Yisu Zhang and Li Tan and Jian Yuan and Rong Tan and Min‐Hua Luo and Fang-Lin Sun and Haipeng Liu and Ying Jiang and Zhiyong Mao},
journal = {Science},
year = {2025},
doi = {10.1126/science.adp5056},
url = {https://doi.org/10.1126/science.adp5056}
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