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dc.contributor.authorRamos, Cayo-
dc.contributor.authorMatas, Isabel M.-
dc.contributor.authorBardaji, Leire-
dc.contributor.authorAragón, Isabel M.-
dc.contributor.authorMurillo, Jesús-
dc.date.accessioned2014-06-03T12:18:34Z-
dc.date.available2014-06-03T12:18:34Z-
dc.date.issued2012-10-24-
dc.identifierdoi: 10.1111/j.1364-3703.2012.00816.x-
dc.identifierissn: 1464-6722-
dc.identifier.citationMolecular Plant Pathology 13(9): 998-1009 (2012)-
dc.identifier.urihttp://hdl.handle.net/10261/97668-
dc.description.abstractPseudomonas savastanoi pv. savastanoi is the causal agent of olive (Olea europaea) knot disease and an unorthodox member of the P. syringae complex, causing aerial tumours instead of the foliar necroses and cankers characteristic of most members of this complex. Olive knot is present wherever olive is grown; although losses are difficult to assess, it is assumed that olive knot is one of the most important diseases of the olive crop. The last century witnessed a large number of scientific articles describing the biology, epidemiology and control of this pathogen. However, most P. savastanoi pv. savastanoi strains are highly recalcitrant to genetic manipulation, which has effectively prevented the pathogen from benefitting from the scientific progress in molecular biology that has elevated the foliar pathogens of the P. syringae complex to supermodels. A number of studies in recent years have made significant advances in the biology, ecology and genetics of P. savastanoi pv. savastanoi, paving the way for the molecular dissection of its interaction with other nonpathogenic bacteria and their woody hosts. The selection of a genetically pliable model strain was soon followed by the development of rapid methods for virulence assessment with micropropagated olive plants and the analysis of cellular interactions with the plant host. The generation of a draft genome of strain NCPPB 3335 and the closed sequence of its three native plasmids has allowed for functional and comparative genomic analyses for the identification of its pathogenicity gene complement. This includes 34 putative type III effector genes and genomic regions, shared with other pathogens of woody hosts, which encode metabolic pathways associated with the degradation of lignin-derived compounds. Now, the time is right to explore the molecular basis of the P. savastanoi pv. savastanoi–olive interaction and to obtain insights into why some pathovars like it necrotic and why some like it knot.-
dc.description.sponsorshipThis work was supported by the Spanish Plan Nacional I Di grants AGL2008-05311-C02-01, AGL2008-05311-C02-02, AGL2011-30343-C02-01 and AGL2011-30343-C02-02 (Ministerio de Economía y Competitividad), co-financed by Fondo Europeo de Desarrollo Regional (FEDER), and by grant P08-CVI-03475 from the Junta de Andalucía, Spain (http://www.juntadeandalucia.es). IMM and IMA were supported by the Ramón Areces Foundation (Spain) and by an FPU fellowship from the Ministerio de Economía y Competitividad (Spain), respectively. We thank L. Rodríguez-Moreno for confocal and electron microscopy images and T. Osinga for help with the English language.-
dc.publisherBlackwell Publishing-
dc.rightsclosedAccess-
dc.titlePseudomonas savastanoi pv. savastanoi: Some like it knot-
dc.typeartículo-
dc.identifier.doi10.1111/j.1364-3703.2012.00816.x-
dc.date.updated2014-06-03T12:18:35Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
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