Abstract
Despite the described central role of jasmonate signaling in plant defense against necrotrophic pathogens, the existence of intraspecific variation in pathogen capacity to activate or evade plant jasmonate-mediated defenses is rarely considered. Experimental infection of jasmonate-deficient and jasmonate-insensitive Arabidopsis thaliana with diverse isolates of the necrotrophic fungal pathogen Botrytis cinerea revealed pathogen variation for virulence inhibition by jasmonate-mediated plant defenses and induction of plant defense metabolites. Comparison of the transcriptional effects of infection by two distinct B. cinerea isolates showed only minor differences in transcriptional responses of wild-type plants, but notable isolate-specific transcript differences in jasmonate-insensitive plants. These transcriptional differences suggest B. cinerea activation of plant defenses that require plant jasmonate signaling for activity in response to only one of the two B. cinerea isolates tested. Thus, similar infection phenotypes observed in wild-type plants result from different signaling interactions with the plant that are likely integrated by jasmonate signaling.
Highlights
Jasmonate-mediated signaling controls diverse aspects of plant growth and defense
To test effects of jasmonate-mediated plant defense on diverse B. cinerea isolates, A. thaliana leaves of the aos genotype and its corresponding wild-type were inoculated with 10 diverse B. cinerea isolates, two abiotic elicitors, or a mock inoculation (Table 1) [41]
While tissue necrosis of aos plants initiated within a time frame similar to wild-type plants, lesions expanded more rapidly in aos plants, with near total consumption of the leaf by B. cinerea between 72 and 96hpi. aos mutant leaves failed to develop the zone of chlorosis surrounding the developing lesion that is often observed in B. cinerea infections (Figure 1A)
Summary
Jasmonate-mediated signaling controls diverse aspects of plant growth and defense. In particular, jasmonate signaling exerts a major influence on plant response to wounding, chewing insects, and necrotrophic pathogens such as Botrytis cinerea, Alternaria brassicicola, Plectosphaerella cucumerina, and Sclerotinia sclerotiorum [1,2,3,4,5,6]. Two major pathogen classes are roughly delineated by the pathogen’s ‘‘lifestyle’’: biotrophic pathogens infect living host cells and necrotrophic pathogens kill cells prior to consuming them [15,16,17]. This difference in the pathogen’s mode of attack strongly influences which signaling networks mediate the plant response. While plants respond to biotrophic and necrotrophic pathogens via different signaling systems, these systems activate common defense responses, such as the production of the A. thaliana defense metabolite, camalexin. Common responses may be controlled by distinct regulatory networks
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