Publication:
Phenotypic and molecular characterization of resistance induction by single and combined application of chitosan and silicon in tomato against Ralstonia solanacearum

dc.bibliographiccitation.firstpage1
dc.bibliographiccitation.journalPhysiological and Molecular Plant Pathology
dc.bibliographiccitation.lastpage12
dc.bibliographiccitation.volume81
dc.contributor.authorKiirika, Leonard Muriithi
dc.contributor.authorStahl, Frank
dc.contributor.authorWydra, Kerstin
dc.date.accessioned2018-11-07T09:30:25Z
dc.date.available2018-11-07T09:30:25Z
dc.date.issued2013
dc.description.abstractSilicon (Si) and chitosan (Chi) treatments induced resistance in tomato against bacterial wilt caused by Ralstonia solanacearum. Gene expression analysis conducted at 72 h post inoculation via TOM2 microarray revealed regulation of 204 and 126 genes in genotypes King Kong 2 and L390, respectively, with their majority classified into the categories defense-related, signal transduction and transcription. In the microarrays, translationally-controlled tumor protein homolog involved in stress reaction of plants, the defense genes chitinases and peroxidases were highly up-regulated in combined Si and Chi treatment. Bacterial wilt incidence was reduced by 40% and 56.6% in Si and Chi treatment, respectively, in King Kong 2, and by 26.6% and 33.3% in Si and Chi treatment, respectively, in L390, and by 74.7% in King Kong 2 and 46.6% in L390 after combined application of Si and Chi. Evidence of their synergistic effects is reported. (C) 2012 Elsevier Ltd. All rights reserved.
dc.identifier.doi10.1016/j.pmpp.2012.11.002
dc.identifier.isi000314814700002
dc.identifier.urihttps://resolver.sub.uni-goettingen.de/purl?gro-2/31301
dc.notes.statuszu prüfen
dc.notes.submitterNajko
dc.publisherAcademic Press Ltd- Elsevier Science Ltd
dc.relation.issn0885-5765
dc.titlePhenotypic and molecular characterization of resistance induction by single and combined application of chitosan and silicon in tomato against Ralstonia solanacearum
dc.typejournal_article
dc.type.internalPublicationyes
dc.type.peerReviewedyes
dc.type.statuspublished
dspace.entity.typePublication

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