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Published on: December 14, 2015
Cyclin D2 is critical for intermediate progenitor cell proliferation in the embryonic cortex
Sara B Glickstein1, Julie A Monaghan, Hajira B Koeller
1Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10021, USA.
Summary
Cyclin D2 (cD2) is crucial for generating cortical progenitor cells. Loss of cD2 impairs progenitor cell division and expansion, impacting brain development. This highlights cD2
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Cyclins D1 (cD1) and D2 (cD2) are expressed in distinct cortical zones.
- A switch to cD2 in progenitor cells is hypothesized to be essential for generating intermediate progenitor cells (IPCs).
Purpose of the Study:
- To investigate the specific role of cyclin D2 (cD2) in the generation and expansion of cortical intermediate progenitor cells (IPCs).
Main Methods:
- Analysis of cyclin D1 and D2 expression in radial glial cells (RGCs) and IPCs.
- Generation and analysis of cD2 and Tbr2 knockout embryonic mouse models.
- Assessment of cell cycle dynamics and progenitor proliferation in mutant cortices.
Main Results:
- Cyclin D2, but not cyclin D1, colabels with Tbr2, a marker for IPCs.
- Loss of cD2 in knockout embryos leads to a reduction in IPCs, microcephaly, and thinning of the cortical subventricular zone (SVZ).
- Absence of cD2 impairs progenitor proliferation and increases cell cycle exit, affecting G1 and S phases.
Conclusions:
- Cyclin D2 plays a critical and non-compensated role in the transition from RGCs to IPCs and supports the expansion of the IPC pool.
- cD2 is essential for maintaining progenitor cell division and regulating cell cycle progression during cortical development.
- The predominant expression of cD2 in the human SVZ suggests its conserved evolutionary importance for generating complex mammalian cortices.
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