Autophagosomes form at ER–mitochondria contact sites

By Maho Hamasaki, Nobumichi Furuta, A. Matsuda, Akiko Nezu, A. Yamamoto, Naonobu Fujita, Hiroko Oomori, Takeshi Noda, T. Haraguchi, Y. Hiraoka and 2 more. Nature, 2013

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Autophagy and multidrug resistance in cancer (2017, background): “The phagophore may be built up from the endoplasmic reticulum-mitochondria contact site [19].”
Autophagy pathway: Cellular and molecular mechanisms (2018, background): “Mitochondria-associated membranes (MAMs), or mitochondria-endoplasmic reticulum contact sites have been implicated in the formation of autophagosomes as potential sites that concentrate ATG formation machinery including ATG14 and STX17.(26) STX17, a Q-SNARE protein mainly resident on ER,(27)”
Atg8 family LC3/GABARAP proteins are crucial for autophagosome–lysosome fusion but not autophagosome formation during PINK1/Parkin mitophagy and starvation (2016, background): “PLE KHM1 is preferentially recruited by GAB ARAPs during PINK1/Parkin mitophagy The autophagosomal soluble N-ethylmaleimide-sensitive factor syntaxin 17 (STX17) has been shown to mediate autophagosome–lysosome fusion (Itakura et al., 2012b; Hamasaki et al., 2013; Diao et al., 2015).”
Autophagy during viral infection — a double-edged sword (2018, background): “The lipid kinase vPS34 creates phosphatidylinositol-3-phosphate (PtdIns3P)-rich regions on the surface of donor membranes, including the endoplasmic reticulum (eR), Golgi apparatus, eR-mitochondria contact sites, endosomes and the plasma membrane [154] [155] [156] [157] [158] .”