Journal
JOURNAL OF CELL BIOLOGY
Volume 193, Issue 2, Pages 397-407Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201004146
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Funding
- European Leukodystrophy Association Foundation
- Institut National de la Sante et de la Recherche Medicale
- Fonds Leon Fredericq
- National Institutes of Health [R01NS045702, P30HD40677]
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The specific functions of intrinsic regulators of oligodendrocyte progenitor cell (OPC) division are poorly understood. Type 2 cyclin-dependent kinase (Cdk2) controls cell cycle progression of OPCs, but whether it acts during myelination and repair of demyelinating lesions remains unexplored. Here, we took advantage of a viable Cdk2(-/-) mutant mouse to investigate the function of this cell cycle regulator in OPC proliferation and differentiation in normal and pathological conditions. During central nervous system (CNS) development, Cdk2 loss does not affect OPC cell cycle, oligodendrocyte cell numbers, or myelination. However, in response to CNS demyelination, it clearly alters adult OPC renewal, cell cycle exit, and differentiation. Importantly, Cdk2 loss accelerates CNS remyelination of demyelinated axons. Thus, Cdk2 is dispensable for myelination but is important for adult OPC renewal, and could be one of the underlying mechanisms that drive adult progenitors to differentiate and thus regenerate myelin.
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