AP2 hemicomplexes contribute independently to synaptic vesicle endocytosis

Mingyu Gu, Qiang Liu, Shigeki Watanabe, Lin Sun, Gunther Hollopeter, Barth D. Grant, Erik M. Jorgensen

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


The clathrin adaptor complex AP2 is thought to be an obligate heterotetramer. We identify null mutations in the α subunit of AP2 in the nematode Caenorhabditis elegans. α-adaptin mutants are viable and the remaining μ2/β hemicomplex retains some function. Conversely, in μ2 mutants, the alpha/sigma2 hemicomplex is localized and is partially functional. α-μ2 double mutants disrupt both halves of the complex and are lethal. The lethality can be rescued by expression of AP2 components in the skin, which allowed us to evaluate the requirement for AP2 subunits at synapses. Mutations in either α or μ2 subunits alone reduce the number of synaptic vesicles by about 30%; however, simultaneous loss of both α and μ2 subunits leads to a 70% reduction in synaptic vesicles and the presence of large vacuoles. These data suggest that AP2 may function as two partially independent hemicomplexes.

Original languageEnglish (US)
Article numbere00190
Issue number2
StatePublished - Mar 5 2013
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology and Microbiology(all)
  • Biochemistry, Genetics and Molecular Biology(all)


Dive into the research topics of 'AP2 hemicomplexes contribute independently to synaptic vesicle endocytosis'. Together they form a unique fingerprint.

Cite this