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Proc Natl Acad Sci U S A. 2009 Jan 27;106(4):1139-44. doi: 10.1073/pnas.0809541106. Epub 2009 Jan 16.

Differential requirements for clathrin in receptor-mediated endocytosis and maintenance of synaptic vesicle pools.

Author information

1
Laboratory of Molecular Traffic, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, 371-8512, Japan. ken@showa.gunma-u.ac.jp

Abstract

Clathrin is a coat protein involved in vesicle budding from several membrane-bound compartments within the cell. Here we present an analysis of a temperature-sensitive (ts) mutant of clathrin heavy chain (CHC) in a multicellular animal. As expected Caenorhabditis elegans chc-1(b1025ts) mutant animals are defective in receptor-mediated endocytosis and arrest development soon after being shifted to the restrictive temperature. Steady-state clathrin levels in these mutants are reduced by more than 95% at all temperatures. Hub interactions and membrane associations are lost at the restrictive temperature. chc-1(b1025ts) animals become paralyzed within minutes of exposure to the restrictive temperature because of a defect in the nervous system. Surprisingly synaptic vesicle number is not reduced in chc-1(b1025ts) animals. Consistent with the normal number of vesicles, postsynaptic miniature currents occur at normal frequencies. Taken together, these results indicate that a high level of CHC activity is required for receptor-mediated endocytosis in nonneuronal cells but is largely dispensable for maintenance of synaptic vesicle pools.

PMID:
19151157
PMCID:
PMC2633560
DOI:
10.1073/pnas.0809541106
[Indexed for MEDLINE]
Free PMC Article

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