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dc.contributor.authorOoi, Cher-Pheng
dc.contributor.authorSmith, Terry K.
dc.contributor.authorGluenz, Eva
dc.contributor.authorWand, Nadina Vasileva
dc.contributor.authorVaughan, Sue
dc.contributor.authorRudenko, Gloria
dc.identifier.citationOoi , C-P , Smith , T K , Gluenz , E , Wand , N V , Vaughan , S & Rudenko , G 2018 , ' Blocking variant surface glycoprotein synthesis alters endoplasmic reticulum exit sites/Golgi homeostasis in Trypanosoma brucei ' , Traffic , vol. Early View .
dc.identifier.otherPURE: 252545988
dc.identifier.otherPURE UUID: 558766b9-eb75-4fa6-beed-4968c08ffc6e
dc.identifier.otherBibtex: urn:ee6f41196e7240fcdf959177a12c58f2
dc.identifier.otherScopus: 85044868880
dc.identifier.otherWOS: 000432037000002
dc.descriptionThis work was supported in part by a Wellcome Trust Senior Research Fellowship award (067441) to T.K.S. G.R. is a Wellcome Senior Fellow in the Basic Biomedical Sciences (095161). This research was funded by the Wellcome Trust.en
dc.description.abstractThe predominant secretory cargo of bloodstream form Trypanosoma brucei is Variant Surface Glycoprotein (VSG), comprising ~10% total protein and forming a dense protective layer. Blocking VSG translation using Morpholino oligonucleotides triggered a precise pre-cytokinesis arrest. We investigated the effect of blocking VSG synthesis on the secretory pathway. The number of Golgi decreased, particularly in post-mitotic cells, from 3.5 ± 0.6 to 2.0 ± 0.04 per cell. Similarly, the number of ER exit sites (ERES) in post-mitotic cells dropped from (3.9 ± 0.6) to (2.7 ± 0.1) eight hours after blocking VSG synthesis. The secretory pathway was still functional in these stalled cells, as monitored using Cathepsin L. Rates of phospholipid and GPI-anchor biosynthesis were relatively unaffected, except for the level of sphingomyelin which increased. However, both ER and Golgi morphology became distorted, with the Golgi cisternae becoming significantly dilated, particularly at the trans-face. Membrane accumulation in these structures is possibly caused by reduced budding of nascent vesicles due to the drastic reduction in the total amount of secretory cargo, i.e. VSG. These data argue that the total flux of secretory cargo impacts upon the biogenesis and maintenance of secretory structures and organelles in T. brucei including the ERES and Golgi.
dc.rights© 2018 The Authors. Traffic published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.en
dc.subjectGolgi biogenesisen
dc.subjectSecretory pathwayen
dc.subjectTrypanosoma bruceien
dc.subjectVariant Surface Glycoproteinen
dc.subjectMembrane metabolismen
dc.subjectER exit siteen
dc.subjectQH301 Biologyen
dc.titleBlocking variant surface glycoprotein synthesis alters endoplasmic reticulum exit sites/Golgi homeostasis in Trypanosoma bruceien
dc.typeJournal articleen
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews.School of Biologyen
dc.contributor.institutionUniversity of St Andrews.Biomedical Sciences Research Complexen
dc.description.statusPeer revieweden

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