Journal
DEVELOPMENTAL CELL
Volume 23, Issue 4, Pages 729-744Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2012.08.006
Keywords
-
Categories
Funding
- Belgian National Funds for Scientific Research
- EMBO long-term fellowships
- Belgian Federation Against Cancer
- Association pour la Recherche sur le Cancer and Ligue Nationale Contre le Cancer
- F.N.R.S.
- Fonds Leon Fredericq
- Fondation Medicale Reine Elisabeth
- Wallon excellence in lifesciences and biotechnology [WELB10]
Ask authors/readers for more resources
The migration of cortical interneurons is characterized by extensive morphological changes that result from successive cycles of nucleokinesis and neurite branching. Their molecular bases remain elusive, and the present work describes how p27(Kip1) controls cell-cycle-unrelated signaling pathways to regulate these morphological remodelings. Live imaging reveals that interneurons lacking p27(Kip1) show delayed tangential migration resulting from defects in both nucleokinesis and dynamic branching of the leading process. At the molecular level, p27(Kip1) is a microtubule-associated protein that promotes polymerization of microtubules in extending neurites, thereby contributing to tangential migration. Furthermore, we show that p27(Kip1) controls actomyosin contractions that drive both forward translocation of the nucleus and growth cone splitting. Thus, p27(Kip1) cell-autonomously controls nucleokinesis and neurite branching by regulating both actin and microtubule cytoskeletons.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available