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Media type:
E-Article
Title:
c-Jun is a negative regulator of myelination
Contributor:
Parkinson, David B.;
Bhaskaran, Ambily;
Arthur-Farraj, Peter;
Noon, Luke A.;
Woodhoo, Ashwin;
Lloyd, Alison C.;
Feltri, M. Laura;
Wrabetz, Lawrence;
Behrens, Axel;
Mirsky, Rhona;
Jessen, Kristján R.
imprint:
Rockefeller University Press, 2008
Published in:The Journal of Cell Biology
Language:
English
DOI:
10.1083/jcb.200803013
ISSN:
1540-8140;
0021-9525
Origination:
Footnote:
Description:
<jats:p>Schwann cell myelination depends on Krox-20/Egr2 and other promyelin transcription factors that are activated by axonal signals and control the generation of myelin-forming cells. Myelin-forming cells remain remarkably plastic and can revert to the immature phenotype, a process which is seen in injured nerves and demyelinating neuropathies. We report that c-Jun is an important regulator of this plasticity. At physiological levels, c-Jun inhibits myelin gene activation by Krox-20 or cyclic adenosine monophosphate. c-Jun also drives myelinating cells back to the immature state in transected nerves in vivo. Enforced c-Jun expression inhibits myelination in cocultures. Furthermore, c-Jun and Krox-20 show a cross-antagonistic functional relationship. c-Jun therefore negatively regulates the myelinating Schwann cell phenotype, representing a signal that functionally stands in opposition to the promyelin transcription factors. Negative regulation of myelination is likely to have significant implications for three areas of Schwann cell biology: the molecular analysis of plasticity, demyelinating pathologies, and the response of peripheral nerves to injury.</jats:p>