Abstract
The first line of defense in plants against pathogens is induced by the recognition of microbe-associated molecular patterns (MAMP). Perception of bacterial flagellin (flg22) by the pattern recognition receptor flagellin-sensing 2 (FLS2) is the best characterized MAMP response, although the underlying molecular mechanisms are not fully understood. Here we studied the relationship between salicylic acid (SA) or jasmonic acid (JA) signaling and FLS2-mediated signaling by monitoring flg22-triggered responses in known SA or JA related mutants of Arabidopsis thaliana (L.) Heynh. The sid2 mutant, impaired in SA biosynthesis, had less basal FLS2 mRNA accumulation than the wild type, which correlated with suppression of early flg22 responses such as ROS production and induction of marker genes, WRKY29 and FRK1. The JA-signaling mutants, jar1 and coi1, exhibited an enhanced flg22-triggered oxidative burst and more callose accumulation than the wild type, and pretreatment with SA or coronatine (COR), a structural mimic of JA-isoleucine, altered these flg22-induced responses. Nonexpressor of pathogenesis-related genes 1 (NPR1) acted downstream of SID2 and required SA-dependent priming for the enhanced flg22-triggered oxidative burst and callose deposition. Activation of JA signaling by COR pretreatment suppressed the flg22-triggered oxidative burst and callose accumulation in a coronatine insensitive 1 (COI1) dependent manner. COR had a negative effect on flg22 responses but only the flg22-triggered oxidative burst depended on SA-JA/COR signaling antagonism. Thus the activated SA and JA signaling pathways have an influence on flg22-triggered oxidative burst and callose deposition. These results may explain how SA and JA signaling are cross talked for regulation of flg22-triggered responses.
Highlights
Current models suggest two forms of innate immunity in plants [1]
Resistance to Pst DC3000 induced by pre-treatment with flg22 was compromised in sid2 plants, demonstrating that flg22-induced salicylic acid (SA) is important for MAMPtriggered resistance [23,52]
Our study points to the impact of SA signaling at an early stage of the flg22 response, oxidative burst that may be involved in late flg22 response, callose deposition
Summary
Current models suggest two forms of innate immunity in plants [1]. In one model, resistance is triggered by microbe-associated molecular patterns (MAMPs) and is referred to as MAMPtriggered immunity (MTI). Flg is a 22-amino acid synthetic polypeptide that corresponds to a highly conserved epitope of the Pseudomonas aeruginosa flagellin protein [2]. It is widely used as a proxy for flagellin in flagellin-mediated signaling in Arabidopsis thaliana (L.) Heynh. Effector-triggered immunity results from the highly specific, direct or indirect interaction of pathogen effectors and the products of plant R genes. This recognition event leads to a strong local defense response that stops pathogen growth [9]
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