The AoPR10 promoter and certain endogenous PR10 genes respond to oxidative signals in Arabidopsis

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Abstract:

SUMMARY

The PR10 class of genes has been associated with plant defence. Previous studies with an asparagus PR10 gene (AoPR1) promoter in heterologous plants suggested that the AoPR10-GUS transgene was responsive to oxidative signals/stresses. Arabidopsis thaliana AoPR10-GUS transgenics allowed expression to be compared with that of a close homologue from the large family of PR10 class genes within the Arabidopsis genome. AoPR10-GUS was induced developmentally at sites of phenylpropanoid accumulation and by wounding, pathogen challenge and treatment with H2O2 but not with salicylic acid (SA), ethylene, methyljasmonate or NO donors. Both wound- and pathogen-associated AoPR10-GUS expression could be suppressed by superoxide dismutase and the NADPH oxidase inhibitor, diphenylene iodonium. Northern blotting using an Arabidopsis PR10 homologue as a probe revealed transcript up-regulation by oxidative species generated by glucose oxidase and xanthine oxidase. In Arabidopsis, the AoPR10-GUS transgene was potentiated by SA and expressed systemically following wounding or challenge with avirulent bacteria. AoPR10-GUS × npr1-1 crosses revealed that potentiation and systemic expression was NPR1-independent. Systemic AoPR10-GUS expression following elicitation of a hypersensitive response but not wounding was abolished in NahG crosses, suggesting an SA-mediated potentiating action during SAR (systemic acquired resistance). These data suggest that the AoPR10 promoter reports the expression of reactive oxygen species-responsive PR10 genes and may indicate systemic changes in oxidative status following either wounding and/or the elicitation of a hypersensitive response in Arabidopsis.

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1364-3703.2004.00244.x

Affiliations: University of Wales Aberystwyth, Institute of Biological Science, Penglais Campus, Aberystwyth SY23 3DA, UK

Publication date: September 1, 2004

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