Abstract
The Arabidopsis constitutive induced resistance 1 (cir1) mutant displays salicylic acid (SA)-dependent constitutive expression of defence genes and enhanced resistance to biotrophic pathogens. To further characterise the role of CIR1 in plant immunity we conducted epistasis analyses with two key components of the SA-signalling branch of the defence network, ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4). We demonstrate that the constitutive defence phenotypes of cir1 require both EDS1 and PAD4, indicating that CIR1 lies upstream of the EDS1-PAD4 regulatory node in the immune signalling network. In light of this finding we examined EDS1 expression in cir1 and observed increased protein, but not mRNA levels in this mutant, suggesting that CIR1 might act as a negative regulator of EDS1 via a post-transcriptional mechanism. Finally, as environmental temperature is known to influence the outcome of plant-pathogen interactions, we analysed cir1 plants grown at 18, 22 or 25°C. We found that susceptibility to Pseudomonas syringae pv. tomato (Pst) DC3000 is modulated by temperature in cir1. Greatest resistance to this pathogen (relative to PR-1:LUC control plants) was observed at 18°C, while at 25°C no difference in susceptibility between cir1 and control plants was apparent. The increase in resistance to Pst DC3000 at 18°C correlated with a stunted growth phenotype, suggesting that activation of defence responses may be enhanced at lower temperatures in the cir1 mutant.
Highlights
Plants have a robust innate immune system that affords protection against attack by potential pathogens in their local environment
We investigated whether the enhanced resistance to Pst DC3000 and H. arabidopsidis and constitutive expression of salicylic acid (SA)-dependent defence genes displayed by the cir1 mutant requires ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4) by generating double mutants
These results are in line with those previously observed for a number of other gain-ofresistance mutants including cpr1, cpr6, bon1, snc1 and suppressor of rps4-RLD 1 [21,22,32,33,34], and indicate that the SARlike constitutive disease resistance displayed by cir1 operates via the EDS1-PAD4 regulatory node
Summary
Plants have a robust innate immune system that affords protection against attack by potential pathogens in their local environment. Recent evidence suggests that EDS1 may play a role in ETI mediated via coiled coil-NB-LRR R proteins, as EDS1 and SA accumulation have been shown to function redundantly in RPS2 and RPP8mediated resistance against avirulent pathogens [12] Both EDS1 and PAD4 are required for SA accumulation in response to Pseudomonas syringe pv. Epistasis analyses have revealed that EDS1 and PAD4 are required for constitutive PR expression and enhanced disease resistance in several cpr mutants including cpr and cpr6 [21,26] Given these results and the pivotal role of the EDS1-PAD4 regulatory node in SA-mediated defence against biotrophic pathogens we investigated whether cir1-mediated resistance to Pst DC3000 and H. arabidopsidis requires EDS1 and/or PAD4, and whether CIR1 might in turn regulate EDS1 expression. We show that the defence and growth phenotypes of the cir mutant are modulated by environmental temperature
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