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NUFIP1整合氨基酸感应和DNA损伤反应以维持肠道稳态。

NUFIP1 integrates amino acid sensing and DNA damage response to maintain the intestinal homeostasis.

作者信息

Ming Hui, Tan Jing, Cao Si-Yi, Yu Cheng-Ping, Qi Yu-Ting, Wang Chao, Zhang Lei, Liu Ying, Yuan Jian, Yin Miao, Lei Qun-Ying

机构信息

Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; School of Basic Medical Sciences, Cancer Institutes; Key Laboratory of Breast Cancer in Shanghai; Shanghai Key Laboratory of Radiation Oncology; the Shanghai Key Laboratory of Medical Epigenetics, State Key Laboratory of Medical Neurobiology, Shanghai Medical College, Fudan University, Shanghai, China.

Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.

出版信息

Nat Metab. 2025 Jan;7(1):120-136. doi: 10.1038/s42255-024-01179-5. Epub 2025 Jan 3.

DOI:10.1038/s42255-024-01179-5
PMID:39753713
Abstract

Nutrient availability strongly affects intestinal homeostasis. Here, we report that low-protein (LP) diets decrease amino acids levels, impair the DNA damage response (DDR), cause DNA damage and exacerbate inflammation in intestinal tissues of male mice with inflammatory bowel disease (IBD). Intriguingly, loss of nuclear fragile X mental retardation-interacting protein 1 (NUFIP1) contributes to the amino acid deficiency-induced impairment of the DDR in vivo and in vitro and induces necroptosis-related spontaneous enteritis. Mechanistically, phosphorylated NUFIP1 binds to replication protein A2 (RPA32) to recruit the ataxia telangiectasia and Rad3-related (ATR)-ATR-interacting protein (ATRIP) complex, triggering the DDR. Consistently, both reintroducing NUFIP1 but not its non-phospho-mutant and inhibition of necroptosis prevent bowel inflammation in male Nufip1 conditional knockout mice. Intestinal inflammation and DNA damage in male mice with IBD can be mitigated by NUFIP1 overexpression. Moreover, NUFIP1 protein levels in the intestine of patients with IBD were found to be significantly decreased. Conclusively, our study uncovers that LP diets contribute to intestinal inflammation by hijacking NUFIP1-DDR signalling and thereby activating necroptosis.

摘要

营养物质的可利用性对肠道稳态有强烈影响。在此,我们报告低蛋白(LP)饮食会降低氨基酸水平,损害DNA损伤反应(DDR),导致DNA损伤,并加剧患有炎症性肠病(IBD)的雄性小鼠肠道组织中的炎症。有趣的是,核脆性X智力低下相互作用蛋白1(NUFIP1)的缺失在体内和体外导致了氨基酸缺乏诱导的DDR损伤,并引发坏死性凋亡相关的自发性肠炎。从机制上讲,磷酸化的NUFIP1与复制蛋白A2(RPA32)结合,以募集共济失调毛细血管扩张症和Rad3相关蛋白(ATR)-ATR相互作用蛋白(ATRIP)复合物,触发DDR。一致地,重新引入NUFIP1而非其非磷酸化突变体以及抑制坏死性凋亡均可预防雄性Nufip1条件性敲除小鼠的肠道炎症。IBD雄性小鼠的肠道炎症和DNA损伤可通过NUFIP1过表达得到缓解。此外,发现IBD患者肠道中NUFIP1蛋白水平显著降低。总之,我们的研究揭示LP饮食通过劫持NUFIP1-DDR信号通路从而激活坏死性凋亡,进而导致肠道炎症。

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