Functionally distinct kinesin-13 family members cooperate to regulate microtubule dynamics during interphase

被引:120
作者
Mennella, V
Rogers, GC
Rogers, SL
Buster, DW
Vale, RD
Sharp, DJ [1 ]
机构
[1] Yeshiva Univ Albert Einstein Coll Med, Dept Physiol & Biophys, Bronx, NY 10461 USA
[2] Univ Calif San Francisco, Dept Mol & Cellular Pharmacol, San Francisco, CA 94107 USA
[3] Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94107 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1038/ncb1222
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Regulation of microtubule polymerization and depolymerization is required for proper cell development. Here, we report that two proteins of the Drosophila melanogaster kinesin-13 family, KLP10A and KLP59C, cooperate to drive microtubule depolymerization in interphase cells. Analyses of microtubule dynamics in S2 cells depleted of these proteins indicate that both proteins stimulate depolymerization, but alter distinct parameters of dynamic instability; KLP10A stimulates catastrophe ( a switch from growth to shrinkage) whereas KLP59C suppresses rescue ( a switch from shrinkage to growth). Moreover, immunofluorescence and live analyses of cells expressing tagged kinesins reveal that KLP10A and KLP59C target to polymerizing and depolymerizing microtubule plus ends, respectively. Our data also suggest that KLP10A is deposited on microtubules by the plus-end tracking protein, EB1. Our findings support a model in which these two members of the kinesin-13 family divide the labour of microtubule depolymerization.
引用
收藏
页码:235 / U39
页数:13
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