Functions of a jumonji–cyclin D1 pathway in the coordination of cell cycle exit and migration during neurogenesis in the mouse hindbrain
During development of the mouse central nervous system (CNS), most neural progenitor cells proliferate in the ventricular zone (VZ). In many regions of the CNS, neural progenitor cells give rise to postmitotic neurons that initiate neuronal differentiation and migrate out of the VZ to the mantle zon...
Saved in:
Published in: | Developmental biology Vol. 303; no. 2; pp. 549 - 560 |
---|---|
Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Elsevier Inc
15-03-2007
|
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | During development of the mouse central nervous system (CNS), most neural progenitor cells proliferate in the ventricular zone (VZ). In many regions of the CNS, neural progenitor cells give rise to postmitotic neurons that initiate neuronal differentiation and migrate out of the VZ to the mantle zone (MZ). Thereafter, they remain in a quiescent state. Here, we found many ectopic mitotic cells and cell clusters expressing neural progenitor or proneural marker genes in the MZ of the hindbrain of
jumonji (
jmj) mutant embryos. When we examined the expression of cyclin D1, which is repressed by
jmj in the repression of cardiac myocyte proliferation, we found many ectopic clusters expressing both cyclin D1 and Musashi 1 in the MZ of mutant embryos.
jmj is mainly expressed in the cyclin D1 negative region in the hindbrain, and cyclin D1 expression in the VZ was upregulated in
jmj mutant mice. In
jmj and
cyclin D1 double mutant mice, the ectopic mitosis and formation of the abnormal clusters in the MZ were rescued. These results suggest that a
jmj–
cyclin D1 pathway is required for the precise coordination of cell cycle exit and migration during neurogenesis in the mouse hindbrain. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0012-1606 1095-564X |
DOI: | 10.1016/j.ydbio.2006.11.031 |