Abstract
Alkamides are fatty acid amides of wide distribution in plants, structurally related to N-acyl-L-homoserine lactones (AHLs) from Gram-negative bacteria and to N- acylethanolamines (NAEs) from plants and mammals. Global analysis of gene expression changes in Arabidopsis thaliana in response to N-isobutyl decanamide, the most highly active alkamide identified to date, revealed an overrepresentation of defense-responsive transcriptional networks. In particular, genes encoding enzymes for jasmonic acid (JA) biosynthesis increased their expression, which occurred in parallel with JA, nitric oxide (NO) and H2O2 accumulation. The activity of the alkamide to confer resistance against the necrotizing fungus Botrytis cinerea was tested by inoculating Arabidopsis detached leaves with conidiospores and evaluating disease symptoms and fungal proliferation. N-isobutyl decanamide application significantly reduced necrosis caused by the pathogen and inhibited fungal proliferation. Arabidopsis mutants jar1 and coi1 altered in JA signaling and a MAP kinase mutant (mpk6), unlike salicylic acid- (SA) related mutant eds16/sid2-1, were unable to defend from fungal attack even when N-isobutyl decanamide was supplied, indicating that alkamides could modulate some necrotrophic-associated defense responses through JA-dependent and MPK6-regulated signaling pathways. Our results suggest a role of alkamides in plant immunity induction.
Highlights
Plants continuously respond to abiotic and biotic stress by adjusting their metabolism and activating diverse intracellular and systemic responses
General defense responses but not salicylic acid biosynthesis are activated by N-isobutyl decanamide Because N-isobutyl decanamide increased the transcript level of a wide class of PR genes, we examined its effect on the production of salicylic acid (SA) and signaling molecules related to local and systemic responses in defense processes
To test whether JA signaling is involved in the N-isobutyl decanamide-induced increased resistance to necrotrophic fungal infection of Arabidopsis leaves, we evaluated the responses of Arabidopsis JA-related mutants jasmonic acid resistant1, coronatine insensitive1, a mutant defective at the MITOGEN-ACTIVATED PROTEIN KINASE6 (MPK6) locus, which has been found to be critical in defense responses to B. cinerea [22], and the SA-related mutant enhanced disease symptoms16
Summary
Plants continuously respond to abiotic and biotic stress by adjusting their metabolism and activating diverse intracellular and systemic responses. Biotic stress induced by pathogens triggers complex signaling cascades regulated by hormones once an invader has been detected. Hormonal-dependent pathways result in the expression of defense-related genes such as those encoding pathogenesis-related (PR) proteins, and the production of antimicrobial secondary metabolites [1]. These responses are assisted by reactive molecules, such as nitric oxide (NO) and reactive oxygen species (ROS) that function both, as signaling components of transcriptional and metabolic readjustment and as antimicrobial substances [2]. The SA-dependent signaling pathway is often considered to be effective against pathogens that derive nutrients from living hosts cells (biotrophs), and JA/ET pathways against pathogens that derive nutrients from dead cells (necrotrophs), the persistence of defense responses and the disease outcome are determined by complex networks of interactions between multiple hormone signaling pathways [3]
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