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p34(cdc2) and mitotic cyclin expression in the developing quail neuroretina
X Espanel1, A Kastner, O Stettler
1Laboratoire de Biologie Moléculaire et Cellulaire de l'Ecole normale supérieure de Lyon, UMR 49 CNRS, Lyon, France.
The International Journal of Developmental Biology
|June 1, 1997
Summary
Central nervous system neurons stop dividing to become postmitotic. This study shows cell cycle regulators like cdc2 decrease as neurons differentiate, suggesting transcriptional control.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- Neurons in the central nervous system (CNS) cease division after development, becoming postmitotic.
- The molecular mechanisms controlling this cell cycle exit are not fully understood.
Purpose of the Study:
- To investigate the molecular events regulating cell cycle exit in developing quail neuroretina.
- To understand the role of cell division control in neuronal differentiation.
Main Methods:
- Analysis of cdc2, cyclin A, and cyclin B2 expression in developing quail neuroretina.
- Immunohistochemical detection of p34(cdc2) and tau protein.
- Monitoring expression of the neuronal differentiation marker beta3-tubulin.
Main Results:
- Expression of cdc2, cyclin A, and cyclin B2 decreases in quail neuroretina between embryonic days 7 and 9.
- Downregulation of p34(cdc2) correlates with the appearance of the microtubule-associated protein tau.
- Postmitotic ganglion cell precursors express beta3-tubulin while p34(cdc2) is still detectable.
Conclusions:
- Inhibition of cdc2 gene expression is linked to terminal neuronal differentiation.
- p34(cdc2) or related kinases may function in early postmitotic neurons during differentiation.