Kinesin-1 regulates dendrite microtubule polarity in Caenorhabditis elegans

Author:

Yan Jing1,Chao Dan L1,Toba Shiori2,Koyasako Kotaro34,Yasunaga Takuo345,Hirotsune Shinji2,Shen Kang1

Affiliation:

1. Department of Biology, Howard Hughes Medical Institute, Stanford University, Stanford, United States

2. Department of Genetic Disease Research, Graduate School of Medicine, Osaka City University, Osaka, Japan

3. Department of Bioscience and Bioinformatics, Faculty of Computer Science and Systems Engineering, Kyushu Institute of Technology, Fukuoka, Japan

4. JST-SENTAN, Japan Science and Technology Agency, Kawaguchi, Japan

5. JST-CREST, Japan Science and Technology Agency, Kawaguchi, Japan

Abstract

In neurons, microtubules (MTs) span the length of both axons and dendrites, and the molecular motors use these intracellular ‘highways' to transport diverse cargo to the appropriate subcellular locations. Whereas axonal MTs are organized such that the plus-end is oriented out from the cell body, dendrites exhibit a mixed MTs polarity containing both minus-end-out and plus-end-out MTs. The molecular mechanisms underlying this differential organization, as well as its functional significance, are unknown. Here, we show that kinesin-1 is critical in establishing the characteristic minus-end-out MT organization of the dendrite in vivo. In unc-116 (kinesin-1/kinesin heavy chain) mutants, the dendritic MTs adopt an axonal-like plus-end-out organization. Kinesin-1 protein is able to cross-link anti-paralleled MTs in vitro. We propose that kinesin-1 regulates the dendrite MT polarity through directly gliding the plus-end-out MTs out of the dendrite using both the motor domain and the C-terminal MT-binding domain.

Funder

Howard Hughes Medical Institute

Human Frontier Science Program

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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