Light is an important modulator of plant immune responses. Here, we show that inactivation of the photoreceptor phytochrome B (phyB) by a low red/far-red ratio (R:FR), which is a signal of competition in plant canopies, down-regulates the expression of defense markers induced by the necrotrophic fungus Botrytis cinerea, including the genes that encode the transcription factor ETHYLENE RESPONSE FACTOR1 (ERF1) and the plant defensin PLANT DEFENSIN1.2 (PDF1.2). This effect of low R:FR correlated with a reduced sensitivity to jasmonate (JA), thus resembling the antagonistic effects of salicylic acid (SA) on JA responses. Low R:FR failed to depress PDF1.2 mRNA levels in a transgenic line in which PDF1.2 transcription was up-regulated by constitutive expression of ERF1 in a coronatine insensitive1 (coi1) mutant background (35S::ERF1/coi1). These results suggest that the low R:FR effect, in contrast to the SA effect, requires a functional SCFCOI1-JASMONATE ZIM-DOMAIN (JAZ) JA receptor module. Furthermore, the effect of low R:FR depressing the JA response was conserved in mutants impaired in SA signaling (sid2-1 and npr1-1). Plant exposure to low R:FR ratios and the phyB mutation markedly increased plant susceptibility to B. cinerea; the effect of low R:FR was (1) independent of the activation of the shade-avoidance syndrome, (2) conserved in the sid2-1 and npr1-1 mutants, and (3) absent in two RNA interference lines disrupted for the expression of the JAZ10 gene. Collectively, our results suggest that low R:FR ratios depress Arabidopsis (Arabidopsis thaliana) immune responses against necrotrophic microorganisms via a SA-independent mechanism that requires the JAZ10 transcriptional repressor and that this effect may increase plant susceptibility to fungal infection in dense canopies.
SummaryHow plants balance resource allocation between growth and defense under conditions of competitive stress is a key question in plant biology. Low red : far-red (R : FR) ratios, which signal a high risk of competition in plant canopies, repress jasmonate-induced defense responses. The mechanism of this repression is not well understood. We addressed this problem in Arabidopsis by investigating the role of DELLA and JASMONATE ZIM domain (JAZ) proteins.We showed that a quintuple della mutant and a phyB mutant were insensitive to jasmonate for several physiological readouts. Inactivation of the photoreceptor phyB by low R : FR ratios rapidly reduced DELLA protein abundance, and the inhibitory effect of FR on jasmonate signaling was missing in the gai-1 mutant, which encodes a stable version of the GAI DELLA protein.We also demonstrated that low R : FR ratios and the phyB mutation stabilized the protein JAZ10. Furthermore, we demonstrated that JAZ10 was required for the inhibitory effect of low R : FR on jasmonate responses, and that the jaz10 mutation restored jasmonate sensitivity to the phyB mutant.We conclude that, under conditions of competition for light, plants redirect resource allocation from defense to rapid elongation by promoting DELLA degradation and enhancing JAZ10 stability.
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