Immune Priming Promotes Thermotolerance, Whereas Thermopriming Suppresses Systemic Acquired Resistance in Arabidopsis.

Abstract

Heat stress and pathogens are two serious yield-limiting factors of crop plants. Plants that previously experienced high but sub-lethal temperatures become subsequently tolerant to higher temperatures through the development of acquired thermotolerance (ATT). ATT activation is associated with the elevated expression of heat shock (HS)-related genes such as HSFA2, HSFA3, and HSP101. Similarly, through the development of systemic acquired resistance (SAR), previously experienced plants achieve a higher resistance than naïve plants. SAR activation requires mobile signals and primarily depends on salicylic acid (SA) signaling. Studies to understand the interaction between ATT and SAR are limiting. To investigate the possible interconnection, we studied cross-protection between SAR and ATT on 4-week-old soil-grown Arabidopsis plants. We observed localized pathogen inoculation provides thermotolerance. Pathogens activate the expressions of HSFA2, HSFA3, HSA32, and HSP101 in pathogen-free systemic tissues. Interestingly, pathogen-induced SAR activation is impaired in hsfa2, hsfa3, and hsp101 mutants, suggesting these HS memory genes are essential for SAR induction. In contrast, thermopriming by exposing plants to sublethal temperatures, blocks SAR activation by pathogens. Thermopriming suppresses SAR mobile signal generation, accumulation of SA, and PR1 gene expression in systemic leaves. Altogether, our results demonstrate a complex interaction between SAR and ATT induction pathways in plants.