id,collection,dc.contributor.author,dc.date.accessioned,dc.date.available,dc.date.issued,dc.description.abstract[en],dc.format.extent,dc.identifier.uri,dc.language,dc.rights.uri,dc.subject.ddc,dc.title,dc.type,dcterms.accessRights.openaire,dcterms.bibliographicCitation,dcterms.bibliographicCitation.doi,dcterms.bibliographicCitation.url,refubium.affiliation[de],refubium.mycore.derivateId,refubium.mycore.fudocsId,refubium.note.author,refubium.resourceType.isindependentpub "408514fb-6089-473a-b6d9-e1be3bf3dc30","fub188/16","Wilhelmi, Ilka||Kanski, Regina||Neumann, Alexander||Herdt, Olga||Hoff, Florian||Jacob, Ralf||Preussner, Marco||Heyd, Florian","2018-06-08T04:00:27Z","2016-10-11T08:06:00.094Z","2016","The transport of secretory proteins from the endoplasmic reticulum (ER) to the Golgi depends on COPII-coated vesicles. While the basic principles of the COPII machinery have been identified, it remains largely unknown how COPII transport is regulated to accommodate tissue- or activation-specific differences in cargo load and identity. Here we show that activation-induced alternative splicing of Sec16 controls adaptation of COPII transport to increased secretory cargo upon T-cell activation. Using splice-site blocking morpholinos and CRISPR/Cas9-mediated genome engineering, we show that the number of ER exit sites, COPII dynamics and transport efficiency depend on Sec16 alternative splicing. As the mechanistic basis, we suggest the C-terminal Sec16 domain to be a splicing-controlled protein interaction platform, with individual isoforms showing differential abilities to recruit COPII components. Our work connects the COPII pathway with alternative splicing, adding a new regulatory layer to protein secretion and its adaptation to changing cellular environments.","14 S.","https://refubium.fu-berlin.de/handle/fub188/16392||http://dx.doi.org/10.17169/refubium-20574","eng","http://creativecommons.org/licenses/by/4.0/","500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie::572 Biochemie","Sec16 alternative splicing dynamically controls COPII transport efficiency","Wissenschaftlicher Artikel","open access","Nature Communications. - 7 (2016), Artikel Nr. 12347","10.1038/ncomms12347","http://www.nature.com/ncomms/2016/160805/ncomms12347/full/ncomms12347.html","Biologie, Chemie, Pharmazie","FUDOCS_derivate_000000006896","FUDOCS_document_000000025138","Der Artikel wurde ine iner Open-Access-Zeitschrift publiziert.","no"