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Mol Plant Microbe Interact ; 25(12): 1584-93, 2012 Dec.
Article in English | MEDLINE | ID: mdl-22950753

ABSTRACT

Plants use different immune pathways to combat pathogens. The activation of the jasmonic acid (JA)-signaling pathway is required for resistance against necrotrophic pathogens; however, to combat biotrophic pathogens, the plants activate mainly the salicylic acid (SA)-signaling pathway. SA can antagonize JA signaling and vice versa. NPR1 (noninducible pathogenesis-related 1) is considered a master regulator of SA signaling. NPR1 interacts with TGA transcription factors, ultimately leading to the activation of SA-dependent responses. SA has been shown to promote disease development caused by the necrotrophic pathogen Botrytis cinerea through NPR1, by suppressing the expression of two JA-dependent defense genes, proteinase inhibitors I and II. We show here that the transcription factor TGA1.a contributes to disease development caused by B. cinerea in tomato by suppressing the expression of proteinase inhibitors I and II. Finally, we present evidence that the SA-signaling pathway contributes to disease development caused by another necrotrophic pathogen, Alternaria solani, in tomato. Disease development promoted by SA through NPR1 requires the TGA1.a transcription factor. These data highlight how necrotrophs manipulate the SAsignaling pathway to promote their disease in tomato.


Subject(s)
Alternaria/pathogenicity , Botrytis/pathogenicity , Plant Diseases/microbiology , Salicylic Acid/metabolism , Signal Transduction , Solanum lycopersicum/microbiology , Cyclopentanes/antagonists & inhibitors , Cyclopentanes/metabolism , Gene Expression Regulation, Plant/drug effects , Host-Pathogen Interactions , Solanum lycopersicum/genetics , Solanum lycopersicum/physiology , Models, Biological , Oxylipins/antagonists & inhibitors , Oxylipins/metabolism , Plant Growth Regulators/metabolism , Plant Immunity , Plant Leaves/genetics , Plant Leaves/microbiology , Plant Leaves/physiology , Plant Proteins/genetics , Plant Proteins/metabolism , Protease Inhibitors , Salicylic Acid/pharmacology , Transcription Factors/genetics , Transcription Factors/metabolism
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