Document Detail

Doublecortin-like kinase controls neurogenesis by regulating mitotic spindles and M phase progression.
MedLine Citation:
PMID:  16387637     Owner:  NLM     Status:  MEDLINE    
The mechanisms controlling neurogenesis during brain development remain relatively unknown. Through a differential protein screen with developmental versus mature neural tissues, we identified a group of developmentally enriched microtubule-associated proteins (MAPs) including doublecortin-like kinase (DCLK), a protein that shares high homology with doublecortin (DCX). DCLK, but not DCX, is highly expressed in regions of active neurogenesis in the neocortex and cerebellum. Through a dynein-dependent mechanism, DCLK regulates the formation of bipolar mitotic spindles and the proper transition from prometaphase to metaphase during mitosis. In cultured cortical neural progenitors, DCLK RNAi Lentivirus disrupts the structure of mitotic spindles and the progression of M phase, causing an increase of cell-cycle exit index and an ectopic commitment to a neuronal fate. Furthermore, both DCLK gain and loss of function in vivo specifically promote a neuronal identity in neural progenitors. These data provide evidence that DCLK controls mitotic division by regulating spindle formation and also determines the fate of neural progenitors during cortical neurogenesis.
Tianzhi Shu; Huang-Chun Tseng; Tamar Sapir; Patrick Stern; Ying Zhou; Kamon Sanada; Andre Fischer; Frédéric M Coquelle; Orly Reiner; Li-Huei Tsai
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Neuron     Volume:  49     ISSN:  0896-6273     ISO Abbreviation:  Neuron     Publication Date:  2006 Jan 
Date Detail:
Created Date:  2006-01-02     Completed Date:  2006-02-14     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8809320     Medline TA:  Neuron     Country:  United States    
Other Details:
Languages:  eng     Pagination:  25-39     Citation Subset:  IM    
Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA.
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MeSH Terms
Cell Differentiation / physiology
Cell Division / physiology*
Cells, Cultured
Cerebral Cortex / embryology
Dyneins / physiology
Embryonic Development / physiology
Microtubule-Associated Proteins / metabolism
Microtubules / physiology
Mitosis / physiology
Mitotic Spindle Apparatus / physiology*
Nervous System / embryology*
Neurons / cytology*,  physiology*
Prometaphase / physiology
Protein-Serine-Threonine Kinases / metabolism,  physiology*
Stem Cells / metabolism
Grant Support
Reg. No./Substance:
0/Microtubule-Associated Proteins; EC 2.7.1.-/Dcamkl1 protein, mouse; EC Kinases; EC
Comment In:
Neuron. 2006 Jan 5;49(1):3-4   [PMID:  16387632 ]

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