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Endonuclease G promotes autophagy by suppressing mTOR signaling and activating the DNA damage response(Open Access)

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收录情况： ◇ SCIE ◇ 自然指数

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机构： [1]The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong [2]Zhuhai Institute of Translational Medicine Zhuhai People’s Hospital Affiliated with Jinan University, Jinan University, Zhuhai, Guangdong [3]The Biomedical Translational Research Institute, Faculty of Medical Science, Jinan University, Guangzhou, Guangdong [4]International Cooperative Laboratory of Traditional Chinese Medicine Modernization and Innovative Drug Development of Chinese Ministry of Education (MOE), College of Pharmacy, Jinan University, Guangzhou, Guangdong [5]Department of Medical Genetics, School of Basic Medicine and Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China [6]Department of Pharmacology & Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR [7]Program in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College Road, Singapore, 169857, Singapore [8]Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA [9]Howard Hughes Medical Institute, Boston, MA

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Endonuclease G (ENDOG), a mitochondrial nuclease, is known to participate in many cellular processes, including apoptosis and paternal mitochondrial elimination, while its role in autophagy remains unclear. Here, we report that ENDOG released from mitochondria promotes autophagy during starvation, which we find to be evolutionally conserved across species by performing experiments in human cell lines, mice, Drosophila and C. elegans. Under starvation, Glycogen synthase kinase 3 beta-mediated phosphorylation of ENDOG at Thr-128 and Ser-288 enhances its interaction with 14-3-3γ, which leads to the release of Tuberin (TSC2) and Phosphatidylinositol 3-kinase catalytic subunit type 3 (Vps34) from 14-3-3γ, followed by mTOR pathway suppression and autophagy initiation. Alternatively, ENDOG activates DNA damage response and triggers autophagy through its endonuclease activity. Our results demonstrate that ENDOG is a crucial regulator of autophagy, manifested by phosphorylation-mediated interaction with 14-3-3γ, and its endonuclease activity-mediated DNA damage response. © 2021, The Author(s).

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出版当年[2020]版：

大类 | 1 区

综合性期刊

小类 | 1 区综合性期刊

最新[2025]版：

大类 | 1 区

综合性期刊

小类 | 1 区综合性期刊

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出版当年[2019]版：

Q1 MULTIDISCIPLINARY SCIENCES

最新[2023]版：

Q1 MULTIDISCIPLINARY SCIENCES

影响因子： 14.7 最新[2023版] 16.1 最新五年平均 12.121 出版当年[2019版] 13.611 出版当年五年平均 11.878 出版前一年[2018版] 14.919 出版后一年[2020版]

第一作者：

第一作者机构： [1]The First Affiliated Hospital, Jinan University, Guangzhou, Guangdong [2]Zhuhai Institute of Translational Medicine Zhuhai People’s Hospital Affiliated with Jinan University, Jinan University, Zhuhai, Guangdong [3]The Biomedical Translational Research Institute, Faculty of Medical Science, Jinan University, Guangzhou, Guangdong

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通讯作者：

通讯机构： [2]Zhuhai Institute of Translational Medicine Zhuhai People’s Hospital Affiliated with Jinan University, Jinan University, Zhuhai, Guangdong [3]The Biomedical Translational Research Institute, Faculty of Medical Science, Jinan University, Guangzhou, Guangdong

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