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Patronin mediates a switch from kinesin-13–dependent poleward flux to anaphase B spindle elongation
Anaphase B spindle elongation contributes to chromosome segregation during Drosophila melanogaster embryo mitosis. We propose that this process is driven by a kinesin-5–generated interpolar microtubule (MT; ipMT) sliding filament mechanism that engages when poleward flux is turned off. In this paper...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3798244/ https://www.ncbi.nlm.nih.gov/pubmed/24100293 http://dx.doi.org/10.1083/jcb.201306001 |
Sumario: | Anaphase B spindle elongation contributes to chromosome segregation during Drosophila melanogaster embryo mitosis. We propose that this process is driven by a kinesin-5–generated interpolar microtubule (MT; ipMT) sliding filament mechanism that engages when poleward flux is turned off. In this paper, we present evidence that anaphase B is induced by the minus end–stabilizing protein Patronin, which antagonizes the kinesin-13 depolymerase KLP10A at spindle poles, thereby switching off the depolymerization of the minus ends of outwardly sliding ipMTs to suppress flux. Although intact cortices, kinetochore MTs, and midzone augmentation are dispensable, this Patronin-based change in ipMT minus-end dynamics is sufficient to induce the elongation of spindles capable of separating chromosomes. |
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