Deletion of Jun proteins in adult oligodendrocytes does not perturb cell survival, or myelin maintenance in vivo.

Schreiner, Bettina; Ingold-Heppner, Barbara; Pehl, Debora; Locatelli, Giuseppe; Berrit-Schönthaler, Helia; Becher, Burkhard (2015). Deletion of Jun proteins in adult oligodendrocytes does not perturb cell survival, or myelin maintenance in vivo. PLoS ONE, 10(3), e0120454. Public Library of Science 10.1371/journal.pone.0120454

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Oligodendrocytes, the myelin-forming glial cells of the central nervous system (CNS), are fundamental players in rapid impulse conduction and normal axonal functions. JunB and c-Jun are DNA-binding components of the AP-1 transcription factor, which is known to regulate different processes such as proliferation, differentiation, stress responses and death in several cell types, including cultured oligodendrocyte/lineage cells. By selectively inactivating Jun B and c-Jun in myelinating oligodendrocytes in vivo, we generated mutant mice that developed normally, and within more than 12 months showed normal ageing and survival rates. In the adult CNS, absence of JunB and c-Jun from mature oligodendrocytes caused low-grade glial activation without overt signs of demyelination or secondary leukocyte infiltration into the brain. Even after exposure to toxic or autoimmune oligodendrocyte insults, signs of altered oligodendrocyte viability were mild and detectable only upon cuprizone treatment. We conclude that JunB and c-Jun expression in post-mitotic oligodendrocytes is mostly dispensable for the maintainance of white matter tracts throughout adult life, even under demyelinating conditions.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Theodor Kocher Institute

UniBE Contributor:

Locatelli, Giuseppe

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1932-6203

Publisher:

Public Library of Science

Language:

English

Submitter:

Ursula Zingg-Zünd

Date Deposited:

22 Mar 2018 16:41

Last Modified:

05 Dec 2022 15:10

Publisher DOI:

10.1371/journal.pone.0120454

PubMed ID:

25774663

BORIS DOI:

10.7892/boris.111249

URI:

https://boris.unibe.ch/id/eprint/111249

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