A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Reference Report

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Citation Rath, U., Rogers, G.C., Tan, D., Gomez-Ferreria, M.A., Buster, D.W., Sosa, H.J., Sharp, D.J. (2009). The Drosophila kinesin-13, KLP59D, impacts Pacman- and Flux-based chromosome movement.  Mol. Biol. Cell 20(22): 4696--4705. (Export to RIS)
FlyBase ID FBrf0209299
Publication Type Research paper
PubMed ID 19793918
PubMed Abstract Chromosome movements are linked to the active depolymerization of spindle microtubule (MT) ends. Here we identify the kinesin-13 family member, KLP59D, as a novel and uniquely important regulator of spindle MT dynamics and chromosome motility in Drosophila somatic cells. During prometaphase and metaphase, depletion of KLP59D, which targets to centrosomes and outer kinetochores, suppresses the depolymerization of spindle pole-associated MT minus ends, thereby inhibiting poleward tubulin Flux. Subsequently, during anaphase, loss of KLP59D strongly attenuates chromatid-to-pole motion by suppressing the depolymerization of both minus and plus ends of kinetochore-associated MTs. The mechanism of KLP59D's impact on spindle MT plus and minus ends appears to differ. Our data support a model in which KLP59D directly depolymerizes kinetochore-associated plus ends during anaphase, but influences minus ends indirectly by localizing the pole-associated MT depolymerase KLP10A. Finally, electron microscopy indicates that, unlike the other Drosophila kinesin-13s, KLP59D is largely incapable of oligomerizing into MT-associated rings in vitro, suggesting that such structures are not a requisite feature of kinetochore-based MT disassembly and chromosome movements.
DOI 10.1091/mbc.E09-07-0557
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Language of Publication English
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Publication Type Journal
Abbreviation Mol. Biol. Cell
Title Molecular Biology of the Cell
Publication Year 1992-
ISBN/ISSN 1059-1524
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