@article {1582731,
	title = {Endonuclease G promotes autophagy by suppressing mTOR signaling and activating the DNA damage response},
	journal = {Nat Commun},
	volume = {12},
	number = {1},
	year = {2021},
	month = {2021 01 20},
	pages = {476},
	abstract = {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.},
	keywords = {14-3-3 Proteins, Animals, Apoptosis, Autophagy, Caenorhabditis elegans, Cell Line, Class III Phosphatidylinositol 3-Kinases, DNA Damage, Drosophila, Endodeoxyribonucleases, Gene Knockout Techniques, Hep G2 Cells, Humans, Liver, Mice, Mice, Knockout, Mitochondria, Phosphorylation, Signal Transduction, TOR Serine-Threonine Kinases, Transcriptome, Tuberous Sclerosis Complex 2 Protein},
	issn = {2041-1723},
	doi = {10.1038/s41467-020-20780-2},
	author = {Wang, Wenjun and Li, Jianshuang and Tan, Junyang and Wang, Miaomiao and Yang, Jing and Zhang, Zhi-Min and Li, Chuanzhou and Basnakian, Alexei G and Tang, Hong-Wen and Perrimon, Norbert and Zhou, Qinghua}
}
