Show simple item record

dc.contributor.authorHirst, Jennifer
dc.contributor.authorEdgar, James R
dc.contributor.authorBorner, Georg HH
dc.contributor.authorLi, Sam
dc.contributor.authorSahlender, Daniela A
dc.contributor.authorAntrobus, Robin
dc.contributor.authorRobinson, Margaret S
dc.date.accessioned2015-09-08T10:07:55Z
dc.date.available2015-09-08T10:07:55Z
dc.date.issued2015-09-01
dc.identifier.citationMolecular Biology of the Cell 2015, 26(17), 3085-3103. doi: 10.1091/mbc.E15-04-0245
dc.identifier.issn1059-1524
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/250528
dc.description.abstractThe precise functions of most of the proteins that participate in clathrin-mediated intracellular trafficking are unknown. We investigated two such proteins, epsinR and gadkin, using the knocksideways method, which rapidly depletes proteins from the available pool by trapping them onto mitochondria. Although epsinR is known to be an N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-specific adaptor, the epsinR knocksideways blocked the production of the entire population of intracellular clathrin-coated vesicles (CCVs), suggesting a more global function. Using the epsinR knocksideways data, we were able to estimate the copy number of all major intracellular CCV proteins. Both sides of the vesicle are densely covered, indicating that CCVs sort their cargo by molecular crowding. Trapping of gadkin onto mitochondria also blocked the production of intracellular CCVs but by a different mechanism: vesicles became cross-linked to mitochondria and pulled out toward the cell periphery. Both phenotypes provide new insights into the regulation of intracellular CCV formation, which could not have been found using more conventional approaches.
dc.languageEnglish
dc.language.isoen
dc.publisherAmerican Society for Cell Biology (ASCB)
dc.rightsAttribution-NonCommercial-ShareAlike 2.0 UK: England & Wales
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/2.0/uk/
dc.titleContributions of epsinR and gadkin to clathrin-mediated intracellular trafficking.
dc.title.alternativeEpsinR, gadkin, and clathrin
dc.typeArticle
dc.description.versionThis is the final version of the article. It first appeared from The American Society for Cell Biology via http://dx.doi.org/10.1091/mbc.E15-04-0245
prism.endingPage3103
prism.publicationDate2015
prism.publicationNameMol Biol Cell
prism.startingPage3085
prism.volume26
dc.rioxxterms.funderWellcome Trust
dcterms.dateAccepted2015-07-06
rioxxterms.versionofrecord10.1091/mbc.E15-04-0245
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2015-07-15
dc.contributor.orcidHirst, Jennifer [0000-0001-9063-8494]
dc.contributor.orcidEdgar, James [0000-0001-7903-8199]
dc.contributor.orcidRobinson, Margaret [0000-0003-0631-0053]
dc.identifier.eissn1939-4586
rioxxterms.typeJournal Article/Review
pubs.funder-project-idWellcome Trust (086598/Z/08/Z)
pubs.funder-project-idWellcome Trust (100140/Z/12/Z)
cam.issuedOnline2015-07-15
rioxxterms.freetoread.startdate2015-09-15


Files in this item

Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-ShareAlike 2.0 UK: England & Wales
Except where otherwise noted, this item's licence is described as Attribution-NonCommercial-ShareAlike 2.0 UK: England & Wales