A predominant issue of global concern is increasing agricultural output to meet the steady rise in global demand. One of the most significant challenges to meeting this objective is overcoming crop loss due to disease and adverse weather. While individual biotic and abiotic stresses are damaging to plants, they can have catastrophic affects when combined, as most often occurs in the field. It has long been observed that environmental conditions, such as temperature and humidity, play a determining role in the outcome of plant-pathogen interactions. Both low and high temperatures have been shown to promote disease depending on the pathosystem involved. Salicylic acid (SA) is a plant hormone important for protection against a broad spectrum of crop-relevant pathogens. However, the direct effect of elevated temperature on SA-mediated defense is unknown. The aims of the research described here were to determine 1) what impact elevated temperature has on SA biosynthesis and signaling, 2) whether observed effects are a direct result of temperature on the host or are also pathogen-dependent and 3) how observed temperature effects on the plant and pathogen interact to determine the final disease outcome. Using the model Arabidopsis thaliana and Pseudomonas syringae pv. tomato DC3000 plant-pathosystem, I present evidence demonstrating that loss of SA biosynthesis and enhanced delivery of bacterial type III effector (T3E) proteins into the plant cells at elevated temperature (30°C) both contribute to enhanced disease.In the host, both SA biosynthesis and signaling are affected in a pathogen-independent manner resulting in enhanced susceptibility. Global transcriptome profiling revealed a temperature-sensitive bifurcation in the SA signaling pathway, with 66% of benzothiadiazole (BTH)-regulated genes, including ISOCHORISMATE SYNTHASE 1 (ICS1) and the widely-used SA marker genes PATHOGENESIS RELATED 1 (PR1), PR2 and PR5, showing compromised expression at 30°C. Surprisingly, BTH-mediated protection against disease is maintained at elevated temperature in spite of the loss of the temperature-sensitive PR1/ICS1 branch of SA-signaling. Exploration of a potential mechanism for SA-mediated protection revealed a novel role of SA in restricting translocation of bacterial T3E into host cells, as translocation was increased in SA-deficient mutants and reduced in BTH-treated plants at 23°C. However, there also seems to be a direct effect of temperature on the pathogen, as T3E translocation was increased more in response to elevated temperature than SA-deficiency.Taken together, these findings support a model whereby elevated temperature acts on both the host, resulting in loss of SA biosynthesis, and on the pathogen, resulting in increased secretion of T3E proteins into plant cells, to promote enhanced bacterial multiplication and disease. Provision of an SA signal, such as BTH, is sufficient to reduce translocation of effector proteins to confer protection against disease. As BTH is used commercially as a crop protectant, the discovery of preserved BTH-mediated protection at elevated temperatures is agriculturally relevant. Furthermore, exploration of the temperature-sensitive and -insensitive branches of SA signaling may also be used to inform genetic approaches to achieve plant resilience to disease under adverse environmental conditions.
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