A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

Reference
Citation Godin, J.D., Colombo, K., Molina-Calavita, M., Keryer, G., Zala, D., Charrin, B.C., Dietrich, P., Volvert, M.L., Guillemot, F., Dragatsis, I., Bellaiche, Y., Saudou, F., Nguyen, L., Humbert, S. (2010). Huntingtin Is Required for Mitotic Spindle Orientation and Mammalian Neurogenesis.  Neuron 67(3): 392--406. (Export to RIS)
FlyBase ID FBrf0211450
Publication Type Research paper
PubMed ID 20696378
PubMed Abstract Huntingtin is the protein mutated in Huntington's disease, a devastating neurodegenerative disorder. We demonstrate here that huntingtin is essential to control mitosis. Huntingtin is localized at spindle poles during mitosis. RNAi-mediated silencing of huntingtin in cells disrupts spindle orientation by mislocalizing the p150(Glued) subunit of dynactin, dynein, and the large nuclear mitotic apparatus NuMA protein. This leads to increased apoptosis following mitosis of adherent cells in vitro. In vivo inactivation of huntingtin by RNAi or by ablation of the Hdh gene affects spindle orientation and cell fate of cortical progenitors of the ventricular zone in mouse embryos. This function is conserved in Drosophila, the specific disruption of Drosophila huntingtin in neuroblast precursors leading to spindle misorientation. Moreover, Drosophila huntingtin restores spindle misorientation in mammalian cells. These findings reveal an unexpected role for huntingtin in dividing cells, with potential important implications in health and disease.
DOI 10.1016/j.neuron.2010.06.027
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Language of Publication English
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Publication Type Journal
Abbreviation Neuron
Title Neuron
Publication Year 1988-
ISBN/ISSN 0896-6273
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