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J Cell Biol. 2014 Mar 31;204(7):1111-21. doi: 10.1083/jcb.201311094.

Ensconsin/Map7 promotes microtubule growth and centrosome separation in Drosophila neural stem cells.

Author information

1
Cytoskeleton and Cell Proliferation, 2 Tubulin and Interacting Proteins, and 3 Spatio-temporal Regulation of Transcription, Biosit, Université de Rennes I, Centre National de la Recherche Scientifique, UMR 6290, 35043 Rennes, France.

Abstract

The mitotic spindle is crucial to achieve segregation of sister chromatids. To identify new mitotic spindle assembly regulators, we isolated 855 microtubule-associated proteins (MAPs) from Drosophila melanogaster mitotic or interphasic embryos. Using RNAi, we screened 96 poorly characterized genes in the Drosophila central nervous system to establish their possible role during spindle assembly. We found that Ensconsin/MAP7 mutant neuroblasts display shorter metaphase spindles, a defect caused by a reduced microtubule polymerization rate and enhanced by centrosome ablation. In agreement with a direct effect in regulating spindle length, Ensconsin overexpression triggered an increase in spindle length in S2 cells, whereas purified Ensconsin stimulated microtubule polymerization in vitro. Interestingly, ensc-null mutant flies also display defective centrosome separation and positioning during interphase, a phenotype also detected in kinesin-1 mutants. Collectively, our results suggest that Ensconsin cooperates with its binding partner Kinesin-1 during interphase to trigger centrosome separation. In addition, Ensconsin promotes microtubule polymerization during mitosis to control spindle length independent of Kinesin-1.

PMID:
24687279
PMCID:
PMC3971751
DOI:
10.1083/jcb.201311094
[Indexed for MEDLINE]
Free PMC Article

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