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Sel1L is essential for the ERAD activity of Sel1L\u2010Hrd1 complex, the best\u2010known ERAD machinery. Using a continuous Sel1L knockout mouse model (<jats:italic>CNP\/Cre<\/jats:italic>; <jats:italic>Sel1L<\/jats:italic><jats:sup><jats:italic>loxP\/loxP<\/jats:italic><\/jats:sup> mice), our previous studies showed that Sel1L knockout in myelinating cells, oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS), leads to adult\u2010onset myelin abnormalities in the CNS and PNS. Because Sel1L is deleted in myelinating cells of <jats:italic>CNP\/Cre<\/jats:italic>; <jats:italic>Sel1L<\/jats:italic><jats:sup><jats:italic>loxP\/loxP<\/jats:italic><\/jats:sup> mice starting at very early stage of differentiation, it is impossible to rule out the possibility that the adult\u2010onset myelin abnormalities in these mice results from developmental myelination defects caused by Sel1L knockout in myelinating cells during development. Thus, using an inducible Sel1L knockout mouse model (<jats:italic>PLP\/CreER<\/jats:italic><jats:sup><jats:italic>T<\/jats:italic><\/jats:sup>; <jats:italic>Sel1L<\/jats:italic><jats:sup><jats:italic>loxP\/loxP<\/jats:italic><\/jats:sup> mice) that has normal, intact myelin and myelinating cells in the adult CNS and PNS prior to tamoxifen treatment, we sought to determine if Sel1L knockout in mature myelinating cells of adult mice leads to myelin abnormalities in the CNS and PNS. We showed that Sel1L knockout in mature myelinating cells caused ERAD impairment, ER stress and UPR activation. Interesting, Sel1L knockout in mature oligodendrocytes impaired their myelinating function by suppressing myelin protein translation, and resulted in progressive myelin thinning in the adult CNS. Conversely, Sel1L knockout in mature Schwann cells led to Schwann cell apoptosis and demyelination in the adult PNS. These findings demonstrate the essential roles of ERAD in mature myelinating cells in the adult CNS and PNS under physiological conditions.<\/jats:p>","DOI":"10.1002\/glia.24346","type":"journal-article","created":{"date-parts":[[2023,1,28]],"date-time":"2023-01-28T12:16:50Z","timestamp":1674908210000},"page":"1360-1376","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Endoplasmic reticulum associated degradation is essential for maintaining the viability or function of mature myelinating cells in adults"],"prefix":"10.1002","volume":"71","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6140-0196","authenticated-orcid":false,"given":"Shuangchan","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Neuroscience University of Minnesota  Minneapolis Minnesota USA"},{"name":"Institute for Translational Neuroscience, University of Minnesota  Minneapolis Minnesota USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4931-7642","authenticated-orcid":false,"given":"Wensheng","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Neuroscience University of Minnesota  Minneapolis Minnesota USA"},{"name":"Institute for Translational Neuroscience, University of Minnesota  Minneapolis Minnesota 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