{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T12:03:20Z","timestamp":1774958600675,"version":"3.50.1"},"reference-count":62,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6577","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[2022,1,14]]},"abstract":"<jats:title>Mitochondria shed their SPOTs<\/jats:title>\n                  <jats:p>\n                    Outer mitochondrial membrane (OMM) function is essential for cellular health. How mitochondria respond to naturally occurring OMM stress is unknown. Li\n                    <jats:italic>et al<\/jats:italic>\n                    . show that, upon infection with the human parasite\n                    <jats:italic>Toxoplasma gondii<\/jats:italic>\n                    , mitochondria shed large structures positive for OMM (SPOTs). SPOT formation required the parasite effector TgMAF1 and its interaction with the host mitochondrial receptor TOM70 and translocase SAM50. TOM70-dependent SPOT formation mediated a depletion of mitochondrial proteins and optimal parasite growth. SPOT-like structures also formed after OMM perturbations independently of infection. Thus, membrane remodeling is a feature of cellular responses to OMM stress that\n                    <jats:italic>Toxoplasma<\/jats:italic>\n                    hijacks during infection. \u2014SMH\n                  <\/jats:p>","DOI":"10.1126\/science.abi4343","type":"journal-article","created":{"date-parts":[[2022,1,14]],"date-time":"2022-01-14T15:36:52Z","timestamp":1642174612000},"source":"Crossref","is-referenced-by-count":93,"title":["Mitochondria shed their outer membrane in response to infection-induced stress"],"prefix":"10.1126","volume":"375","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1099-518X","authenticated-orcid":true,"given":"Xianhe","family":"Li","sequence":"first","affiliation":[{"name":"Max Planck Institute for Biology of Ageing, Cologne, Germany."}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4544-6332","authenticated-orcid":true,"given":"Julian","family":"Straub","sequence":"additional","affiliation":[{"name":"Max Planck Institute for Biology of Ageing, 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