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dc.contributor.authorSurve, Sachin V.
dc.contributor.authorJensen, Brian C.
dc.contributor.authorHeestand, Meredith
dc.contributor.authorMazet, Muriel
dc.contributor.authorSmith, Terry K.
dc.contributor.authorBringaud, Frédéric
dc.contributor.authorParsons, Marilyn
dc.contributor.authorSchnaufer, Achim
dc.date.accessioned2017-01-06T10:30:11Z
dc.date.available2017-01-06T10:30:11Z
dc.date.issued2017-01
dc.identifier.citationSurve , S V , Jensen , B C , Heestand , M , Mazet , M , Smith , T K , Bringaud , F , Parsons , M & Schnaufer , A 2017 , ' NADH dehydrogenase of Trypanosoma brucei is important for efficient acetate production in bloodstream forms ' Molecular and Biochemical Parasitology , vol. 211 , pp. 57-61 . DOI: 10.1016/j.molbiopara.2016.10.001en
dc.identifier.issn0166-6851
dc.identifier.otherPURE: 246519707
dc.identifier.otherPURE UUID: ad759722-3279-4ed3-ab1e-3cff7a0c9f54
dc.identifier.otherRIS: urn:7D91C85DE6933C10203D9A42E5167E3F
dc.identifier.otherScopus: 84994389388
dc.identifier.urihttp://hdl.handle.net/10023/10052
dc.descriptionThis work was supported by a grant from the National Institutes of Health (USA) [AI 5R01 AI069057] to MP and AS; a grant from the Medical Research Council (UK) [G0600129] to AS; grants from the Centre National de la Recherche Scientifique (CNRS, France), The Université de Bordeaux, The Agence Nationale de la Recherche (ANR) [ACETOTRYP of the ANR-BLANC-2010 call and GLYCONOV of the “Générique” call] and the Laboratoire d’Excellence (LabEx) ParaFrap [grant ANR-11-LABX-0024] to FB; and a grant from the Wellcome Trust [093228] to TKS.en
dc.description.abstractIn the slender bloodstream form, Trypanosoma brucei mitochondria are repressed for many functions. Multiple components of mitochondrial complex I, NADH:ubiquinone oxidoreductase, are expressed in this stage, but electron transfer through complex I is not essential. Here we investigate the role of the parasite’s second NADH:ubiquinone oxidoreductase, NDH2, which is composed of a single subunit that also localizes to the mitochondrion. While inducible knockdown of NDH2 had a modest growth effect in bloodstream forms, NDH2 null mutants, as well as inducible knockdowns in a complex I deficient background, showed a greater reduction in growth. Altering the NAD+/NADH balance would affect numerous processes directly and indirectly, including acetate production. Indeed, loss of NDH2 led to reduced levels of acetate, which is required for several essential pathways in bloodstream form T. brucei and which may have contributed to the observed growth defect. In conclusion our study shows that NDH2 is important, but not essential, in proliferating bloodstream forms of T. brucei, arguing that the mitochondrial NAD+/NADH balance is important in this stage, even though the mitochondrion itself is not actively engaged in the generation of ATP.en
dc.format.extent5en
dc.language.isoeng
dc.relation.ispartofMolecular and Biochemical Parasitologyen
dc.rights© 2016 The Authors. Published by Elsevier B.V. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).en
dc.subjectTrypanosoma bruceien
dc.subjectMitochondrionen
dc.subjectNDH2en
dc.subjectRespiratory complex Ien
dc.subjectNADH:ubiquinone oxidoreductaseen
dc.subjectAcetateen
dc.subjectQH301 Biologyen
dc.subjectQD Chemistryen
dc.subjectNDASen
dc.subject.lccQH301en
dc.subject.lccQDen
dc.titleNADH dehydrogenase of Trypanosoma brucei is important for efficient acetate production in bloodstream formsen
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.identifier.doihttps://doi.org/10.1016/j.molbiopara.2016.10.001
dc.description.statusPeer revieweden


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