Document Detail


Cell cycle regulation during mouse olfactory neurogenesis.
MedLine Citation:
PMID:  11751454     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The development of the nervous system requires a strict control of cell cycle entry and withdrawal. The olfactory epithelium (OE) is noticeable by its ability to yield new neurons not only during development but also continuously during adulthood. The aim of our study was to investigate, by biochemical and immunohistochemical methods, which cell cycle regulators are involved in the control of neuron production during OE development and maturity. At birth, olfactory neural progenitors, the basal cells, exhibited a high mitogenic and neurogenic activity, decreasing in the following weeks together with the drop in expression of several cell cycle regulators. p27Kip1 and p18Ink4c, at birth, were expressed in the whole basal cell layer, whereas p16Ink4a, p19Ink4d, and p21Cip1 were rather located in differentiating or mature neurons. CDK inhibitors may thus act sequentially during this developmental neurogenic process. By comparison, in the adult OE, in which most neural precursors were quiescent, these cells still exhibited p18Ink4c expression but only occasionally p27Kip1 expression. It suggests that p18Ink4c may contribute to maintain basal cells in a quiescent state, whereas p27Kip1 expression in these cells may be rather linked to their neurogenic activity, which declines with age. In keeping with this hypothesis, transgenic mice that lacked p27Kip1 expression displayed a higher rate of cell proliferation versus differentiation in their OE. In these mice, a down-regulation of positive cell cycle regulators was observed that may contribute to compensate for the absence of p27Kip1. Taken together, the present data suggest distinct functions for CDK inhibitors, either in the control of cell cycle exit and differentiation during neurogenesis (respectively, p27Kip1 and p19Ink4d) or in the maintenance of a quiescent state in neural progenitors (p18Ink4c) or neurons (p21Cip1) in adults.
Authors:
M E Legrier; A Ducray; A Propper; M Chao; A Kastner
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research     Volume:  12     ISSN:  1044-9523     ISO Abbreviation:  Cell Growth Differ.     Publication Date:  2001 Dec 
Date Detail:
Created Date:  2001-12-25     Completed Date:  2002-03-04     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  9100024     Medline TA:  Cell Growth Differ     Country:  United States    
Other Details:
Languages:  eng     Pagination:  591-601     Citation Subset:  IM    
Affiliation:
Laboratoire de neurosciences, EA481, Université de Franche-Comté, 25 030 Besançon Cedex, France.
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MeSH Terms
Descriptor/Qualifier:
Age Factors
Animals
Blotting, Western
Cell Cycle
Cell Cycle Proteins / metabolism*
Cell Division
Cyclin-Dependent Kinase Inhibitor p16 / metabolism*
Cyclin-Dependent Kinase Inhibitor p18
Cyclin-Dependent Kinase Inhibitor p19
Cyclin-Dependent Kinase Inhibitor p21
Cyclin-Dependent Kinase Inhibitor p27
Cyclins / metabolism*
Down-Regulation
Enzyme Inhibitors / metabolism*,  pharmacology
Immunohistochemistry
Kinetics
Mice
Neurons / metabolism*
Olfactory Bulb / embryology*,  metabolism*
Olfactory Mucosa / metabolism
Protein Binding
Time Factors
Tumor Suppressor Proteins / metabolism*
Chemical
Reg. No./Substance:
0/Cdkn1a protein, mouse; 0/Cdkn1b protein, mouse; 0/Cdkn2c protein, mouse; 0/Cdkn2d protein, mouse; 0/Cell Cycle Proteins; 0/Cyclin-Dependent Kinase Inhibitor p16; 0/Cyclin-Dependent Kinase Inhibitor p18; 0/Cyclin-Dependent Kinase Inhibitor p19; 0/Cyclin-Dependent Kinase Inhibitor p21; 0/Cyclins; 0/Enzyme Inhibitors; 0/Tumor Suppressor Proteins; 147604-94-2/Cyclin-Dependent Kinase Inhibitor p27

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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