{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T05:15:14Z","timestamp":1790745314839,"version":"4.1.0"},"reference-count":57,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2022,8,17]],"date-time":"2022-08-17T00:00:00Z","timestamp":1660694400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Biology of the Cell"],"published-print":{"date-parts":[[2022,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background Information<\/jats:title>\n                    <jats:p>Mitofusin2 (MFN2), an important molecular player that regulates mitochondrial fusion, also helps maintain the inter\u2010organellar contact sites, referred as mitochondria associated membranes (MAMs) that exist between the ER and mitochondria. The study deals with a mutant of MFN2, R364W\u2010MFN2, linked with the neuropathy, Charcot Marie Tooth (CMT) disease. Previous studies show that this mutant promotes mitochondrial hyperfusion. Here, we try to decipher the role of R364W\u2010MFN2 in affecting the ER mitochondrial associations at the MAM junctions and inter\u2010organellar calcium signalling between the ER and the mitochondria.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Our results show that R364W\u2010MFN2 altered ER\u2010mitochondria association at the MAM junctions, predisposed mitochondria towards cellular stress with the mitochondria undergoing rapid fission upon induction of mild stress and perturbs inter\u2010organellar calcium homeostasis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      The results indicate that R364W\u2010MFN2 not only affects mitochondrial morphology and dynamics but also modulate its interaction with the ER and Ca\n                      <jats:sup>2+<\/jats:sup>\n                      signalling between the two organelles.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance<\/jats:title>\n                    <jats:p>This study provides significant insight that presence of the R364W\u2010MFN2 mutation makes cells susceptible towards stress, thus negatively affecting cellular health which altogether might culminate in the form of the CMT neuropathy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/boc.202100098","type":"journal-article","created":{"date-parts":[[2022,8,4]],"date-time":"2022-08-04T05:28:55Z","timestamp":1659590935000},"page":"309-319","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["CMT2A\u2010linked mitochondrial hyperfusion\u2010driving mutant MFN2 perturbs ER\u2010mitochondrial associations and Ca\n                    <sup>2+<\/sup>\n  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