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CMTM5 - a novel CNS myelin protein involved in preserving axonal integrity

dc.contributor.advisorWerner, Hauke Dr.
dc.contributor.authorBuscham, Tobias
dc.date.accessioned2022-04-28T12:52:46Z
dc.date.available2022-05-03T00:50:11Z
dc.date.issued2022-04-28
dc.identifier.urihttp://resolver.sub.uni-goettingen.de/purl?ediss-11858/14016
dc.identifier.urihttp://dx.doi.org/10.53846/goediss-9213
dc.language.isoengde
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subject.ddc570de
dc.titleCMTM5 - a novel CNS myelin protein involved in preserving axonal integrityde
dc.typedoctoralThesisde
dc.contributor.refereeWerner, Hauke Dr.
dc.date.examination2022-04-07de
dc.description.abstractengMyelination of axons in the nervous system facilitates rapid, saltatory signal propagation, accelerating nerve conduction speed manyfold. Additionally, myelinating glia support the long-term integrity of axons they enwrap. However, the relevance of many myelin proteins in these processes has remained elusive. In this study we identify CMTM5 (Chemokine-like factor-like MARVEL-transmembrane domain containing protein 5) as a low abundant but highly specific constituent of CNS myelin. We find that genetic disruption of the Cmtm5-gene in myelinating glial cells in mice does not alter myelin development or ultrastructure. However, deletion of Cmtm5 in oligodendrocytes causes a progressive axonopathy in the CNS that is ameliorated by presence of the Wlds mutation, suggesting a Wallerian like mechanism of axon degeneration. Ablation of Cmtm5 in myelinating Schwann cells of the PNS leads to a reduction in axonal diameters without evident axonal pathology, suggesting that CMTM5 serves different roles in the CNS and the PNS, respectively. Our results indicate that CMTM5 is not crucial for myelin biogenesis, structure, or composition but contributes to the functions of oligodendrocytes in maintaining axonal integrity in the CNS.de
dc.contributor.coRefereeBoretius, Susann Prof. Dr.
dc.subject.engCMTMde
dc.subject.engOligodendrocytede
dc.subject.engMyelinde
dc.subject.engAxonopathyde
dc.identifier.urnurn:nbn:de:gbv:7-ediss-14016-6
dc.affiliation.instituteBiologische Fakultät für Biologie und Psychologiede
dc.subject.gokfullBiologie (PPN619462639)de
dc.description.embargoed2022-05-03de
dc.identifier.ppn1800601158


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