Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/51040

Full metadata record
DC FieldValueLanguage
dc.contributor.authorTrindade, Dario Alexandre Martinspor
dc.contributor.authorPereira, Clara Isabel Ferreirapor
dc.contributor.authorChaves, Susana Alexandra Rodriguespor
dc.contributor.authorManon, Stephenpor
dc.contributor.authorCôrte-Real, Manuelapor
dc.contributor.authorSousa, Maria Joãopor
dc.date.accessioned2018-02-26T11:38:39Z-
dc.date.issued2016-10-
dc.date.submitted2016-02-
dc.identifier.citationTrindade, D., Pereira, C., Chaves, S. R., Manon, S., Côrte-Real, M., & Sousa, M. J. (2016). VDAC regulates AAC-mediated apoptosis and cytochrome c release in yeast. Microbial Cell, 3(10), 500por
dc.identifier.issn2311-2638por
dc.identifier.urihttp://hdl.handle.net/1822/51040-
dc.description.abstractMitochondrial outer membrane permeabilization is a key event in apoptosis processes leading to the release of lethal factors. We have previously shown that absence of the ADP/ATP carrier (AAC) proteins (yeast orthologues of mammalian ANT proteins) increased the resistance of yeast cells to acetic acid, preventing MOMP and the release of cytochrome c from mitochondria during acetic acid – induced apoptosis. On the other hand, deletion of POR1 (yeast voltage-dependent anion channel – VDAC) increased the sensitivity of yeast cells to acetic acid. In the present work, we aimed to further characterize the role of yeast VDAC in acetic acid – induced apoptosis and assess if it functionally interacts with AAC proteins. We found that the sensitivity to acetic acid resulting from POR1 deletion is completely abrogated by the absence of AAC proteins, and propose that Por1p acts as a negative regulator of acetic acid – induced cell death by a mechanism dependent of AAC proteins, by acting on AAC – dependent cytochrome c release. Moreover, we show that Por1p has a role in mitochondrial fusion that, contrary to its role in apoptosis, is not affected by the absence of AAC, and demonstrate that mitochondrial network fragmentation is not sufficient to induce release of cytochrome c or sensitivity to acetic acid – induced apoptosis. This work enhances our understanding on cytochrome c release during cell death, which may be relevant in pathological scenarios where MOMP is compromisedpor
dc.description.sponsorshipNew York, USA, for providing the yeast strain W303. D. Trindade was the recipient of a fellowship from Fundação Calouste Gulbenkian, Portugal. Work at the Institut de Biochimie et Génétique Cellulaires (IBGC), CNRS/Université Bordeaux Segalen was supported by Fundação Calouste Gulbenkian. This work was supported by FCT I.P through the strategic programme UID/BIA/04050/2013, project FCT-ANR/BEX-BCM/0175/2012 and a fellowship to S. Chaves (SFRH/ BPD/89980/2012)por
dc.language.isoengpor
dc.publisherShared Science Publisherspor
dc.rightsrestrictedAccesspor
dc.subjectAACpor
dc.subjectPor1por
dc.subjectMitochondriapor
dc.subjectCytochrome cpor
dc.subjectAcetic acidpor
dc.subjectApoptosispor
dc.titleVDAC regulates AAC-mediated apoptosis and cytochrome c release in yeastpor
dc.typearticlepor
dc.peerreviewedyespor
dc.relation.publisherversionhttp://microbialcell.com/researcharticles/vdac-regulates-aac-mediated-apoptosis-and-cytochrome-c-release-in-yeast/por
oaire.citationStartPage500por
oaire.citationEndPage510por
oaire.citationIssue10por
oaire.citationVolume3por
dc.identifier.essn2311-2638por
dc.identifier.doi10.15698/mic2016.10.533por
dc.subject.fosEngenharia e Tecnologia::Biotecnologia Industrialpor
dc.description.publicationversioninfo:eu-repo/semantics/publishedVersionpor
dc.subject.wosScience & Technologypor
sdum.journalMicrobial Cellpor
Appears in Collections:DBio - Artigos/Papers

Files in This Item:
File Description SizeFormat 
Trindade et al 2016-1.pdf
  Restricted access
552,14 kBAdobe PDFView/Open

Partilhe no FacebookPartilhe no TwitterPartilhe no DeliciousPartilhe no LinkedInPartilhe no DiggAdicionar ao Google BookmarksPartilhe no MySpacePartilhe no Orkut
Exporte no formato BibTex mendeley Exporte no formato Endnote Adicione ao seu ORCID