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dc.contributor.authorDíaz de la Loza, María del Carmen
dc.contributor.authorGallardo, Mercedes
dc.contributor.authorGarcía-Rubio, María Luisa
dc.contributor.authorIzquierdo, Alicia
dc.contributor.authorHerrero Perpiñán, Enrique
dc.contributor.authorAguilera, Andrés
dc.contributor.authorWellinger, Ralf Erik
dc.date.accessioned2012-12-10T13:36:20Z
dc.date.available2012-12-10T13:36:20Z
dc.date.issued2011
dc.identifier.issn0305-1048
dc.identifier.urihttp://hdl.handle.net/10459.1/46367
dc.description.abstractGenomic instability is related to a wide-range of human diseases. Here, we show that mitochondrial iron–sulfur cluster biosynthesis is important for the maintenance of nuclear genome stability in Saccharomyces cerevisiae. Cells lacking the mitochondrial chaperone Zim17 (Tim15/Hep1), a component of the iron–sulfur biosynthesis machinery, have limited respiration activity, mimic the metabolic response to iron starvation and suffer a dramatic increase in nuclear genome recombination. Increased oxidative damage or deficient DNA repair do not account for the observed genomic hyperrecombination. Impaired cell-cycle progression and genetic interactions of ZIM17 with components of the RFC-like complex involved in mitotic checkpoints indicate that replicative stress causes hyperrecombination in zim17Δ mutants. Furthermore, nuclear accumulation of pre-ribosomal particles in zim17Δ mutants reinforces the importance of iron–sulfur clusters in normal ribosome biosynthesis. We propose that compromised ribosome biosynthesis and cell-cycle progression are interconnected, together contributing to replicative stress and nuclear genome instability in zim17Δ mutants.ca_ES
dc.description.sponsorshipEuropean Union (EUROFAN II to A.A.); Spanish Ministry of Science and Innovation (BIO2003-07172 and BIO2006-08051 to R.E.W. and Consolider Ingenio 2010, CSD2007-0015); Junta de Andalucía (P08-CTS-04297 to R.E.W.); Pre-doctoral FPI fellowship from the Spanish Ministry of Science and Innovation (to M.D.L.). Funding for open access charge: Proyecto de investigación de excelencia (P08-CTS-04297) of the Junta de Andalucía.
dc.language.isoengca_ES
dc.publisherOxford University Pressca_ES
dc.relationMICYT/PN2000-2003/BIO2003-07172
dc.relationMIECI/PN2004-2007/BIO2006-08051
dc.relationMIECI/PN2004-2007/CSD2007-0015
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.1093/nar/gkr193ca_ES
dc.relation.ispartofNucleic Acids Research, 2011, vol. 39, núm. 14, p. 6002-6015ca_ES
dc.rightscc-by-nc, (c) Díaz de la Loza et al., 2011ca_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc/2.5/es/deed.ca
dc.subjectIron-Sulfur Proteins
dc.subjectMitochondrial proteins
dc.subjectSaccharomyces cerevisiae proteins
dc.subjectZim 17 protein
dc.subject.otherLlevat de cervesaca_ES
dc.subject.otherExpressió gènica
dc.subject.otherFerro
dc.titleZim17/Tim15 links mitochondrial iron–sulfur cluster biosynthesis to nuclear genome stabilityca_ES
dc.typearticleca_ES
dc.identifier.idgrec016913
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1093/nar/gkr193


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cc-by-nc, (c) Díaz de la Loza et al., 2011
Except where otherwise noted, this item's license is described as cc-by-nc, (c) Díaz de la Loza et al., 2011