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Malfunctions within the ER\u2013mitochondria contacts altering lipid trafficking homeostasis manifest in diverse pathologies, but the molecular effectors governing this process remain ill-defined. Here, we report that PERK promotes lipid trafficking at the ER\u2013mitochondria contact sites (EMCS) through a non-conventional, unfolded protein response-independent, mechanism. PERK operates as an adaptor for the recruitment of the ER\u2013plasma membrane tether and lipid transfer protein (LTP) Extended-Synaptotagmin 1 (E-Syt1), within the EMCS. In resting cells, the heterotypic E-Syt1-PERK interaction endorses transfer of PLs between the ER and mitochondria. Weakening the E-Syt1-PERK interaction or removing the lipid transfer SMP-domain of E-Syt1, compromises mitochondrial respiration. Our findings unravel E-Syt1 as a PERK interacting LTP and molecular component of the lipid trafficking machinery of the EMCS, which critically maintains mitochondrial homeostasis and fitness.<\/jats:p>","DOI":"10.1083\/jcb.202206008","type":"journal-article","created":{"date-parts":[[2023,1,20]],"date-time":"2023-01-20T02:21:21Z","timestamp":1674181281000},"update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":68,"title":["PERK recruits E-Syt1 at ER\u2013mitochondria contacts for mitochondrial lipid transport and respiration"],"prefix":"10.1083","volume":"222","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2262-6915","authenticated-orcid":true,"given":"Maria Livia","family":"Sassano","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05f950310","id-type":"ROR","asserted-by":"publisher"}],"name":"Cell Death Research and Therapy Group, Department of Cellular and Molecular Medicine, KU Leuven 1 , Leuven, 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