Kinesin-1 Regulates Microtubule Dynamics via a c-Jun N-terminal Kinase-dependent Mechanism

被引:49
作者
Daire, Vanessa [4 ]
Giustiniani, Julien
Leroy-Gori, Ingrid
Quesnoit, Melanie [2 ,3 ]
Drevensek, Stephanie
Dimitrov, Ariane [2 ,3 ]
Perez, Franck [2 ,3 ]
Poues, Christian [1 ,5 ]
机构
[1] Univ Paris 11, Fac Pharm, JE2493, IFR141, F-92296 Chatenay Malabry, France
[2] CNRS, UMR 144, F-75246 Paris 05, France
[3] Inst Curie, Sect Rech, F-75246 Paris 05, France
[4] Univ Paris Sud, Pharm Galen & Biopharm Lab, CNRS, Fac Pharm,IFR141,UMR BioCis 8076, F-92296 Chatenay Malabry, France
[5] Hop Antoine Beclere, AP HP, F-92141 Clamart, France
关键词
PLUS-END; MOTOR PROTEINS; IN-VIVO; PHOSPHORYLATION; BINDING; MOTILITY; GROWTH; INSTABILITY; ASSOCIATION; MODULATION;
D O I
10.1074/jbc.M109.007906
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In the kinesin family, all the molecular motors that have been implicated in the regulation of microtubule dynamics have been shown to stimulate microtubule depolymerization. Here, we report that kinesin-1 (also known as conventional kinesin or KIF5B) stimulates microtubule elongation and rescues. We show that microtubule-associated kinesin-1 carries the c-Jun N-terminal kinase (JNK) to allow its activation and that microtubule elongation requires JNK activity throughout the microtubule life cycle. We also show that kinesin-1 and JNK promoted microtubule rescues to similar extents. Stimulation of microtubule rescues by the kinesin-1/JNK pathway could not be accounted for by the rescue factor CLIP-170. Indeed only a dual inhibition of kinesin-1/JNK and CLIP-170 completely blocked rescues and led to extensive microtubule loss. We propose that the kinesin-1/JNK signaling pathway is a major regulator of microtubule dynamics in living cells and that it is required with the rescue factor CLIP-170 to allow cells to build their interphase microtubule network.
引用
收藏
页码:31992 / 32001
页数:10
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