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dc.contributor.authorPérez-Martín, Martaes_ES
dc.contributor.authorBably-Haas,Crysten E.es_ES
dc.contributor.authorPérez-Pérez, María Estheres_ES
dc.contributor.authorAndrés-Garrido, Ascensiónes_ES
dc.contributor.authorBlaby, Ian K.es_ES
dc.contributor.authorMerchant, Sabeeha S.es_ES
dc.contributor.authorCejudo, Francisco Javieres_ES
dc.date.accessioned2015-09-10T06:33:31Z-
dc.date.available2015-09-10T06:33:31Z-
dc.date.issued2015-
dc.identifier.citationEukaryotic Cell, 14(9): 964-973 (2015)es_ES
dc.identifier.urihttp://hdl.handle.net/10261/121887-
dc.description.abstractAutophagy is an intracellular self-degradation pathway by which eukaryotic cells recycle their own material in response to specific stress conditions. Exposure to high concentrations of metals causes cell damage, although the effect of metal stress on autophagy has not been explored in photosynthetic organisms. In this study, we investigated the effect of metal excess on autophagy in the model unicellular green alga Chlamydomonas reinhardtii. We show in cells treated with nickel an upregulation of ATG8 that is independent of CRR1, a global regulator of copper signaling in Chlamydomonas. A similar effect on ATG8 was observed with copper and cobalt but not with cadmium or mercury ions. Transcriptome sequencing data revealed an increase in the abundance of the protein degradation machinery, including that responsible for autophagy, and a substantial overlap of that increased abundance with the hydrogen peroxide response in cells treated with nickel ions. Thus, our results indicate that metal stress triggers autophagy in Chlamydomonas and suggest that excess nickel may cause oxidative damage, which in turn activates degradative pathways, including autophagy, to clear impaired components and recover cellular homeostasises_ES
dc.language.isoenges_ES
dc.publisherASM Internationales_ES
dc.relation.isversionofPublisher's versiones_ES
dc.rightsopenAccesses_ES
dc.titleActivation of Autophagy by Metals in Chlamydomonas reinhardtiies_ES
dc.typeartículoes_ES
dc.identifier.doi10.1128/EC.00081-15.-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1128/EC.00081-15.es_ES
dc.relation.csices_ES
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