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

Ken Sato, Glen G. Ernstrom, Shigeki Watanabe, Robby M. Weimer, Chih Hsiung Chen, Miyuki Sato, Ayesha Siddiqui, Erik M. Jorgensen, Barth D. Grant

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish (US)
Pages (from-to)1139-1144
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume106
Issue number4
DOIs
StatePublished - Jan 27 2009
Externally publishedYes

Keywords

  • Caenorhabditis elegans
  • Synapse

ASJC Scopus subject areas

  • General

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