Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 30, Issue 11, Pages 2737-2749Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.01566-09
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Funding
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- Commissariat al'Energie Atomique (CEA)
- Ligue Nationale Contre le Cancer (Equipe Labelisee) [2007]
- Institut National du Cancer [57]
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Genetic programs that govern neural stem/progenitor cell (NSC) proliferation and differentiation are dependent on extracellular cues and a network of transcription factors, which can be regulated posttranslationally by phosphorylation. However, little is known about the kinase-dependent pathways regulating NSC maintenance and oligodendrocyte development. We used a conditional knockout approach to target the murine regulatory subunit (beta) of protein kinase casein kinase 2 (CK2 beta) in embryonic neural progenitors. Loss of CK2 beta leads to defects in proliferation and differentiation of embryonic NSCs. We establish CK2 beta as a key positive regulator for the development of oligodendrocyte precursor cells (OPCs), both in vivo and in vitro. We show that CK2 beta directly interacts with the basic helix-loop-helix (bHLH) transcription factor Olig2, a critical modulator of OPC development, and activates the CK2-dependent phosphorylation of its serine-threonine-rich (STR) domain. Finally, we reveal that the CK2-targeted STR domain is required for the oligodendroglial function of Olig2. These findings suggest that CK2 may control oligodendrogenesis, in part, by regulating the activity of the lineage-specific transcription factor Olig2. Thus, CK2 beta appears to play an essential and uncompensated role in central nervous system development.
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