Suppression of UDP-glycosyltransferase-coding Arabidopsis thaliana UGT74E2 Gene Expression Leads to Increased Resistance to Psuedomonas syringae pv. tomato DC3000 Infection

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Plants possess multiple resistance mechanisms that protect themselves against pathogen attack. To identify unknown components of the defense machinery in Arabidopsis, gene-expression changes were monitored in Arabidopsis thaliana under 18 different biotic or abiotic conditions using a DNA microarray representing approximately 25% of all Arabidopsis thaliana genes (www.genevestigator.com). Seventeen genes which are early responsive to salicylic acid (SA) treatment as well as pathogen infection were selected and their T-DNA insertion mutants were obtained from SALK institute. To elucidate the role of each gene in defense response, bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000 was inoculated onto individual T-DNA insertion mutants. Four mutants exhibited decreased resistance and five mutants displayed significantly enhanced resistance against Psi DC3000-infection as measured by change in symptom development as compared to wild-type plants. Among them, member of uridin diphosphate (UDP)-glycosyltransferase (UGT) was of particular interest, since a UGT mutant (At1g05680) showed enhanced resistance to Psi-infection in Arabidopsis. In systemic acquired resistance (SAR) assay, this mutant showed enhanced activation of SAR. Also, the enhanced SAR correlated with increased expression of defense-related gene, AtPR1. These results emphasize that the glycosylation of UGT74E2 is a part of the SA-mediated disease-resistance mechanism.
Publisher
KOREAN SOC PLANT PATHOLOGY
Issue Date
2011-06
Language
English
Article Type
Article
Keywords

SYSTEMIC ACQUIRED-RESISTANCE; SALICYLIC-ACID GLUCOSYLTRANSFERASE; DISEASE RESISTANCE; PLANT DEFENSE; METHYL SALICYLATE; VIRUS-RESISTANCE; CROSS-TALK; TOBACCO; GLUCOSE; NPR1

Citation

PLANT PATHOLOGY JOURNAL, v.27, no.2, pp.170 - 182

ISSN
1598-2254
DOI
10.5423/PPJ.2011.27.2.170
URI
http://hdl.handle.net/10203/255593
Appears in Collection
RIMS Journal Papers
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