Salicylic acid dependent signaling promotes basal thermotolerance but is not essential for acquired thermotolerance in <i>Arabidopsis thaliana</i>

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<jats:title>Summary</jats:title><jats:p>Salicylic acid (SA) is reported to protect plants from heat shock (HS), but insufficient is known about its role in thermotolerance or how this relates to SA signaling in pathogen resistance. We tested thermotolerance and expression of pathogenesis‐related (PR) and HS proteins (HSPs) in <jats:italic>Arabidopsis thaliana</jats:italic> genotypes with modified SA signaling: plants with the SA hydroxylase <jats:italic>NahG</jats:italic> transgene, the <jats:styled-content>n</jats:styled-content>onexpresser of <jats:styled-content>PR</jats:styled-content> proteins (<jats:italic>npr1</jats:italic>) mutant, and the <jats:styled-content>c</jats:styled-content>onstitutive expressers of <jats:styled-content>PR</jats:styled-content> proteins (<jats:italic>cpr1</jats:italic> and <jats:italic>cpr5</jats:italic>) mutants. At all growth stages from seeds to 3‐week‐old plants, we found evidence for SA‐dependent signaling in basal thermotolerance (i.e. tolerance of HS without prior heat acclimation). Endogenous SA correlated with basal thermotolerance, with the SA‐deficient <jats:italic>NahG</jats:italic> and SA‐accumulating <jats:italic>cpr5</jats:italic> genotypes having lowest and highest thermotolerance, respectively. SA promoted thermotolerance during the HS itself and subsequent recovery. Recovery from HS apparently involved an NPR1‐dependent pathway but thermotolerance during HS did not. SA reduced electrolyte leakage, indicating that it induced membrane thermoprotection. <jats:italic>PR‐1</jats:italic> and <jats:italic>Hsp17.6</jats:italic> were induced by SA or HS, indicating common factors in pathogen and HS responses. SA‐induced <jats:italic>Hsp17.6</jats:italic> expression had a different dose–response to <jats:italic>PR‐1</jats:italic> expression. HS‐induced Hsp17.6 protein appeared more slowly in <jats:italic>NahG</jats:italic>. However, SA only partially induced HSPs. <jats:italic>Hsp17.6</jats:italic> induction by HS was more substantial than by SA, and we found no SA effect on <jats:italic>Hsp101</jats:italic> expression. All genotypes, including <jats:italic>NahG</jats:italic> and <jats:italic>npr1</jats:italic>, were capable of expression of HSPs and acquisition of HS tolerance by prior heat acclimation. Although SA promotes basal thermotolerance, it is not essential for acquired thermotolerance.</jats:p>

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