A post-docking role for active zone protein Rim

Sandhya P. Koushika, Janet E. Richmond, Gayla Hadwiger, Robby M. Weimer, Erik M. Jorgensen, Michael L. Nonet

Research output: Contribution to journalArticle

233 Scopus citations

Abstract

Rim1 was previously identified as a Rab3 effector localized to the presynaptic active zone in vertebrates. Here we demonstrate that C. elegans unc-10 mutants lacking Rim are viable, but exhibit behavioral and physiological defects that are more severe than those of Rab3 mutants. Rim is localized to synaptic sites in C. elegans, but the ultrastructure of the presynaptic densities is normal in Rim mutants. Moreover, normal levels of docked synaptic vesicles were observed in mutants, suggesting that Rim is not involved in the docking process. The level of fusion competent vesicles at release sites was reduced fivefold in Rim mutants, but calcium sensitivity of release events was unchanged. Furthermore, expression of a constitutively open form of syntaxin suppressed the physiological defects of Rim mutants, suggesting Rim normally acts to regulate conformational changes in syntaxin. These data suggest Rim acts after vesicle docking likely via regulating priming.

Original languageEnglish
Pages (from-to)997-1005
Number of pages9
JournalNature neuroscience
Volume4
Issue number10
DOIs
StatePublished - Oct 14 2001

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    Koushika, S. P., Richmond, J. E., Hadwiger, G., Weimer, R. M., Jorgensen, E. M., & Nonet, M. L. (2001). A post-docking role for active zone protein Rim. Nature neuroscience, 4(10), 997-1005. https://doi.org/10.1038/nn732