Please use this identifier to cite or link to this item: https://doi.org/10.1242/bio.20148276
Title: The kinesin-13 KLP10A motor regulates oocyte spindle length and affects EB1 binding without altering microtubule growth rates
Authors: Do, K.K
Hoàng, K.L
Endow, S.A 
Issue Date: 2014
Citation: Do, K.K, Hoàng, K.L, Endow, S.A (2014). The kinesin-13 KLP10A motor regulates oocyte spindle length and affects EB1 binding without altering microtubule growth rates. Biology Open 3 (7) : 561-570. ScholarBank@NUS Repository. https://doi.org/10.1242/bio.20148276
Rights: Attribution 4.0 International
Abstract: Kinesin-13 motors are unusual in that they do not walk along microtubules, but instead diffuse to the ends, where they remove tubulin dimers, regulating microtubule dynamics. Here we show that Drosophila kinesin-13 klp10A regulates oocyte meiosis I spindle length and is haplo-insufficient - KLP10A, reduced by RNAi or a loss-of-function P element insertion mutant, results in elongated and mispositioned oocyte spindles, and abnormal cortical microtubule asters and aggregates. KLP10A knockdown by RNAi does not significantly affect microtubule growth rates in oocyte spindles, but, unexpectedly, EB1 binding and unbinding are slowed, suggesting a previously unobserved role for kinesin-13 in mediating EB1 binding interactions with microtubules. Kinesin-13 may regulate spindle length both by disassembling subunits from microtubule ends and facilitating EB1 binding to plus ends. We also observe an increased number of paused microtubules in klp10A RNAi knockdown spindles, consistent with a reduced frequency of microtubule catastrophes. Overall, our findings indicate that reduced kinesin-13 decreases microtubule disassembly rates and affects EB1 interactions with microtubules, rather than altering microtubule growth rates, causing spindles to elongate and abnormal cortical microtubule asters and aggregates to form. © 2014, Company of Biologists Ltd. All rights reserved.
Source Title: Biology Open
URI: https://scholarbank.nus.edu.sg/handle/10635/182022
ISSN: 20466390
DOI: 10.1242/bio.20148276
Rights: Attribution 4.0 International
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