Cyclin-Dependent Kinase-2 Controls Oligodendrocyte Progenitor Cell Cycle Progression and Is Downregulated in Adult Oligodendrocyte Progenitors

• DOI: 10.1523/jneurosci.22-19-08553.2002
• Publication Date: 2018-04-03T20:25:16Z
• Authors: Shibeshih Belachew; Adan A. Aguirre; Hang Wang; François Vautier; Xiaoqing Yuan; Stacie Anderson; Martha Kirby; Vittorio Gallo
• Keywords: Cyclin E; Cyclin A; Cyclin A2; Cyclin D2

Proliferation of oligodendrocyte progenitor (OP) cells is a crucial process controlling myelination in the CNS. Previous studies demonstrated correlation between OP proliferation rate and cyclin E/cyclin-dependent kinase-2 (cdk2) activity. To establish causal link E/cdk2 activity proliferation, we selectively modulated cdk2 <i>in vitro</i> by transfection cultured cells. Dominant-negative (Dn)-cdk2 overexpression inhibited mitogen-induced cell whereas wild-type (wt)-cdk2 prevented cycle arrest caused anti-mitotic signals. Dn-cdk2- or wt-cdk2-mediated regulation G₁/S transition, per se, did not influence initiation differentiation. study function during development vivo</i>, analyzed E expression acutely isolated from transgenic mice expressing green fluorescent protein (GFP) under control 2′-3′-cyclic nucleotide 3′-phosphodiesterase gene promoter. Both levels were decreased GFP⁺oligodendrocyte lineage postnatal days 4 30. Immunostaining NG2⁺/GFP⁺ brain tissue sections showed 90% decrease overall perinatal adult However, within proliferating (i.e., nuclear antigen) population was maintained throughout development. Our data indicate that: (1) plays pivotal decisions occurring at checkpoint; (2) differentiation independent cyclinE/cdk2 checkpoint, (3) intrinsic differences may underlie slowly proliferative state that characterizes so-called "quiescent" vivo</i>.