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The Cdc42-selective GAP Rich regulates postsynaptic development and retrograde BMP transsynaptic signaling

Cited 35 time in Web of Science Cited 35 time in Scopus
Authors
Nahm, Minyeop; Long, A. Ashleigh; Paik, Sang Kyoo; Kim, Sungdae; Broadie, Kendal; Lee, Seungbok; Bae, Yong Chul
Issue Date
2010-11-01
Publisher
ROCKEFELLER UNIV PRESS
Citation
JOURNAL OF CELL BIOLOGY; Vol.191, No.3, pp.661-675
Abstract
Retrograde bone morphogenetic protein signaling mediated by the Glass bottom boat (Gbb) ligand modulates structural and functional synaptogenesis at the Drosophila melanogaster neuromuscular junction However, the molecular mechanisms regulating post synaptic Gbb release are poorly understood In this study, we show that Drosophila Rich (dRich), a conserved Cdc42-selective guanosine triphosphatase activating protein (GAP), inhibits the Cdc42-Wsp pathway to stimulate postsynaptic Gbb release Loss of dRich causes synaptic undergrowth and strongly impairs neurotransmitter release These presynaptic defects are rescued by targeted postsynaptic expression of wild type dRich but not a GAP-deficient mutant dRich inhibits the post synaptic localization of the Cdc42 effector Wsp (Drosophila orthologue of mammalian Wiskott Aldrich syndrome protein, WASp), and manifestation of synaptogenesis defects in drich mutants requires Wsp signaling In addition, dRich regulates postsynaptic organization independently of Cdc42 Importantly, dRich increases Gbb release and elevates presynaptic phosphorylated Mad levels We propose that dRich coordinates the Gbb dependent modulation of synaptic growth and function with postsynaptic development
ISSN
0021-9525
Language
English
URI
https://hdl.handle.net/10371/80400
DOI
https://doi.org/10.1083/jcb.201007086
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College of Dentistry/School of Dentistry (치과대학/치의학대학원)Dept. of Dentistry (치의학과)Journal Papers (저널논문_치의학과)
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