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Published online November 5, 2007
doi:10.1083/jcb.200702036
The Journal of Cell Biology, Vol. 179, No. 3, 539-552
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Huang et al.
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Article

 Very-KIND, a KIND domain–containing RasGEF, controls dendrite growth by linking Ras small GTPases and MAP2

Jinhong Huang, Asako Furuya, and Teiichi Furuichi

Laboratory for Molecular Neurogenesis, RIKEN Brain Science Institute, Wako, Saitama 351-0198, Japan

Correspondence to Teiichi Furuichi: tfuruichi{at}brain.riken.jp

The regulation of cytoskeletal components in the dendritic shaft core is critical for dendrite elongation and branching. Here, we report that a brain-specific Ras guanine nucleotide exchange factor (RasGEF) carrying two kinase non-catalytic C-lobe domains (KINDs), very-KIND (v-KIND), regulates microtubule-associated protein 2 (MAP2). v-KIND is expressed in developing mouse brain, predominantly in the cerebellar granule cells. v-KIND not only activates Ras small GTPases via the C-terminal RasGEF domain, but also specifically binds to MAP2 via the second KIND domain (KIND2), leading to threonine phosphorylation of MAP2. v-KIND overexpression suppresses dendritic extension and branching of hippocampal neurons and cerebellar granule cells, whereas knockdown of endogenous v-KIND expression promotes dendrite growth. These findings suggest that v-KIND mediates a signaling pathway that links Ras and MAP2 to control dendrite growth.

J. Huang's present address is Drug Discovery Research Lab, Hanno Research Center, TAIHO Pharmaceutical Co., Ltd., 1-27, Misugidai, Hanno-shi, Saitama, 357-8527, Japan.

Abbreviations used in this paper: DIV, days in vitro; GEF, guanine nucleotide exchange factor; HMW MAP2, high molecular weight MAP2; KINDs, kinase non-catalytic C-terminal domains; MAP2, microtubule associated protein 2; MT, microtubule; v-KIND, very-KIND.


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