Journal
NEURON
Volume 67, Issue 3, Pages 392-406Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2010.06.027
Keywords
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Funding
- Agence Nationale pour la Recherche [ANR-07-BLAN-3-207540, ANR-09-BLAN-0080, ANR-08-MNP-039]
- Association pour la Recherche sur le Cancer (ARC) [4830, 3665]
- Fondation pour la Recherche Medicate (FRM)
- Fondation BNP Paribas
- F.R.S.-F.N.R.S.
- Fonds Leon Fredericq
- Fondation Medicate Reine Elisabeth
- CNRS
- INSERM
- ERC [CePoDro 209718]
- Curie Institute
- Region Ile de France
- Ligue Nationale contre le Cancer and EMBO
- Institut Curie Foreign Student
- FRM
- Swiss National Science Foundation
- HighQ foundation
- Agence Nationale de la Recherche (ANR) [ANR-09-BLAN-0080] Funding Source: Agence Nationale de la Recherche (ANR)
- Medical Research Council [MC_U117570528] Funding Source: researchfish
- MRC [MC_U117570528] Funding Source: UKRI
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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.
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