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Published on: January 12, 2015
Disruption of CK2beta in embryonic neural stem cells compromises proliferation and oligodendrogenesis in the mouse
Emmanuelle Huillard1, Léa Ziercher, Olivier Blond
1INSERM, U873, CEA, iRTSV/LTS, 17 Av. des Martyrs, F-38054 Grenoble, France.
Abstract:
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 (CK2beta) in embryonic neural progenitors. Loss of CK2beta leads to defects in proliferation and differentiation of embryonic NSCs. We establish CK2beta as a key positive regulator for the development of oligodendrocyte precursor cells (OPCs), both in vivo and in vitro. We show that CK2beta 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, CK2beta appears to play an essential and uncompensated role in central nervous system development.
Insights
Protein kinase CK2beta is crucial for neural stem cell development and oligodendrocyte precursor cell formation. It regulates Olig2 transcription factor activity, essential for central nervous system development.
Area of Science:
- Neuroscience
- Molecular Biology
- Cell Biology
Background:
- Neural stem cell (NSC) proliferation and differentiation depend on extracellular signals and transcription factors.
- Posttranslational modifications, like phosphorylation, regulate transcription factor activity.
- Kinase pathways governing NSC maintenance and oligodendrocyte development are poorly understood.
Purpose of the Study:
- To investigate the role of protein kinase casein kinase 2 beta (CK2beta) in neural stem/progenitor cell (NSC) regulation.
- To determine CK2beta's function in oligodendrocyte precursor cell (OPC) development.
- To elucidate the interaction between CK2beta and the transcription factor Olig2.
Main Methods:
- Conditional knockout of CK2beta in murine embryonic neural progenitors.
- In vivo and in vitro studies of NSC proliferation and differentiation.
- Analysis of CK2beta interaction with Olig2 and its phosphorylation status.
Main Results:
- Loss of CK2beta impairs embryonic NSC proliferation and differentiation.
- CK2beta is a key positive regulator of oligodendrocyte precursor cell (OPC) development.
- CK2beta directly interacts with and phosphorylates the transcription factor Olig2.
- Phosphorylation of Olig2's serine-threonine-rich domain by CK2 is essential for oligodendroglial function.
Conclusions:
- CK2beta plays an essential, uncompensated role in central nervous system development.
- CK2 regulates oligodendrogenesis partly through modulating Olig2 activity.
- CK2beta is vital for maintaining neural stem cell function and promoting oligodendrocyte differentiation.
