Methyl Salicylate Production and Jasmonate Signaling Are Not Essential for Systemic Acquired Resistance inArabidopsis 

Abstract

Systemic acquired resistance (SAR) develops in response to local microbial leaf inoculation and renders the whole plant more resistant to subsequent pathogen infection. Accumulation of salicylic acid (SA) in noninfected plant parts is required for SAR, and methyl salicylate (MeSA) and jasmonate (JA) are proposed to have critical roles during SAR long-distance signaling from inoculated to distant leaves. Here, we address the significance of MeSA and JA during SAR development in Arabidopsis thaliana. MeSA production increases in leaves inoculated with the SAR-inducing bacterial pathogen Pseudomonas syringae; however, most MeSA is emitted into the atmosphere, and only small amounts are retained. We show that in several Arabidopsis defense mutants, the abilities to produce MeSA and to establish SAR do not coincide. T-DNA insertion lines defective in expression of a pathogen-responsive SA methyltransferase gene are completely devoid of induced MeSA production but increase systemic SA levels and develop SAR upon local P. syringae inoculation. Therefore, MeSA is dispensable for SAR in Arabidopsis, and SA accumulation in distant leaves appears to occur by de novo synthesis via isochorismate synthase. We show that MeSA production induced by P. syringae depends on the JA pathway but that JA biosynthesis or downstream signaling is not required for SAR. In compatible interactions, MeSA production depends on the P. syringae virulence factor coronatine, suggesting that the phytopathogen uses coronatine-mediated volatilization of MeSA from leaves to attenuate the SA-based defense pathway.

Impact of root exudates and plant defense signaling on bacterial communities in the rhizosphere. A review

“…In a search for this mobile signal, it was proposed that locally produced SA is esterified to methyl salicylate (MeSA), which is transported to systemic tissues and there converted back to SA (Seskar et al 1998;Park et al 2007). However, Attaran et al (2009) demonstrated that in Arabidopsis the synthesis of MeSA does not coincide with the expression of SAR. Earlier, Maldonado et al (2002) suggested that a lipidbased molecule could function as the long-distance regulator of SAR in Arabidopsis.…”

“…Moreover, a recent study by Jung et al (2009) suggests azelaic acid to be the transported mobile signal required for the systemic activation of SAR in Arabidopsis. Although also JA signaling occurs in the early response of SAR, JA biosynthesis, or downstream signaling are not required for the systemic expression of SAR (Truman et al 2007;Vlot et al 2008;Attaran et al 2009). …”

Arabidopsis AZI1 family proteins mediate signal mobilization for systemic defence priming

“…The existence of more than one signal capable of establishing a primed state suggests that plants may use a consortium of molecules to reach a certain 'priming threshold'. Responses to specific signals can depend on plant growth/infection conditions, which highlights the plasticity of plant responses 10,14,16,[20][21][22] .…”

Salicylic Acid-Dependent Plant Stress Signaling via Mitochondrial Succinate Dehydrogenase

“…Accumulation of SA is often correlated with an increase in ROS production during plant stress response (for review, see Herrera-Vásquez et al, 2015). A series of SA binding proteins has been identified, notably catalase (Chen et al, 1993a), peroxidase (Durner and Klessig, 1995), and methyl-salicylate esterase (Forouhar et al, 2005) that appear to explain this correlation, but their roles as general SA receptors have been controversial (Attaran et al, 2009;Bi et al, 1995). Further sets of SA binding proteins in Arabidopsis have been identified by affinity screens and include several mitochondrial enzymes and also GSTs including GSTF8, which showed enzymatic inhibition by SA (Manohar et al, 2015;Tian et al, 2012).…”