{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Buscham TJ"],"funding":["Deutsche Forschungsgemeinschaft","European Research Council","Wellcome Trust"],"pagination":["e75523"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8916772"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11"],"pubmed_abstract":["Oligodendrocytes facilitate rapid impulse propagation along the axons they myelinate and support their long-term integrity. However, the functional relevance of many myelin proteins has remained unknown. Here, we find that expression of the tetraspan-transmembrane protein CMTM5 (chemokine-like factor-like MARVEL-transmembrane domain containing protein 5) is highly enriched in oligodendrocytes and central nervous system (CNS) myelin. Genetic disruption of the <i>Cmtm5</i> gene in oligodendrocytes of mice does not impair the development or ultrastructure of CNS myelin. However, oligodendroglial <i>Cmtm5</i> deficiency causes an early-onset progressive axonopathy, which we also observe in global and tamoxifen-induced oligodendroglial <i>Cmtm5</i> mutants. Presence of the <i>Wld<sup>S</sup></i> mutation ameliorates the axonopathy, implying a Wallerian degeneration-like pathomechanism. These results indicate that CMTM5 is involved in the function of oligodendrocytes to maintain axonal integrity rather than myelin biogenesis."],"journal":["eLife"],"pubmed_title":["Progressive axonopathy when oligodendrocytes lack the myelin protein CMTM5."],"pmcid":["PMC8916772"],"funding_grant_id":["Advanced Grant MyeliNano","WE 2720/2-2","WE 2720/4-1","WE 2720/5-1"],"pubmed_authors":["Steyer AM","Boretius S","Jahn O","Buscham TJ","Strenzke N","Siems SB","Dardawal R","Sun T","Nave KA","Eichel-Vogel MA","Memhave TR","Werner HB","Muller C","Mobius W","Ruhwedel T","Meschkat M","Kramer-Albers EM"],"additional_accession":[]},"is_claimable":false,"name":"Progressive axonopathy when oligodendrocytes lack the myelin protein CMTM5.","description":"Oligodendrocytes facilitate rapid impulse propagation along the axons they myelinate and support their long-term integrity. However, the functional relevance of many myelin proteins has remained unknown. Here, we find that expression of the tetraspan-transmembrane protein CMTM5 (chemokine-like factor-like MARVEL-transmembrane domain containing protein 5) is highly enriched in oligodendrocytes and central nervous system (CNS) myelin. Genetic disruption of the <i>Cmtm5</i> gene in oligodendrocytes of mice does not impair the development or ultrastructure of CNS myelin. However, oligodendroglial <i>Cmtm5</i> deficiency causes an early-onset progressive axonopathy, which we also observe in global and tamoxifen-induced oligodendroglial <i>Cmtm5</i> mutants. Presence of the <i>Wld<sup>S</sup></i> mutation ameliorates the axonopathy, implying a Wallerian degeneration-like pathomechanism. These results indicate that CMTM5 is involved in the function of oligodendrocytes to maintain axonal integrity rather than myelin biogenesis.","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2026-05-31T05:00:23.451Z","creation":"2026-04-08T08:10:10.803Z"},"accession":"S-EPMC8916772","cross_references":{"pubmed":["35274615"],"doi":["10.7554/eLife.75523"]}}