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Extreme weather conditions associated with climate change affect many aspects of plant and animal life, including the response to infectious diseases. Production of salicylic acid (SA), a central plant defence hormone 1 – 3 , is particularly vulnerable to suppression by short periods of hot weather above the normal plant growth temperature range via an unknown mechanism 4 – 7 . Here we show that suppression of SA production in Arabidopsis thaliana at 28 °C is independent of PHYTOCHROME B 8 , 9 (phyB) and EARLY FLOWERING 3 10 (ELF3), which regulate thermo-responsive plant growth and development. Instead, we found that formation of GUANYLATE BINDING PROTEIN-LIKE 3 (GBPL3) defence-activated biomolecular condensates 11 (GDACs) was reduced at the higher growth temperature. The altered GDAC formation in vivo is linked to impaired recruitment of GBPL3 and SA-associated Mediator subunits to the promoters of CBP60g and SARD1 , which encode master immune transcription factors. Unlike many other SA signalling components, including the SA receptor and biosynthetic genes, optimized CBP60g expression was sufficient to broadly restore SA production, basal immunity and effector-triggered immunity at the elevated growth temperature without significant growth trade-offs. CBP60g family transcription factors are widely conserved in plants 12 . These results have implications for safeguarding the plant immune system as well as understanding the concept of the plant–pathogen–environment disease triangle and the emergence of new disease epidemics in a warming climate. Suppression of salicylic acid production in  Arabidopsis thaliana at high temperature is caused by decreased recruitment of GUANYLATE BINDING PROTEIN-LIKE 3 defence-associated condensates on promoter sites of master immune regulatory genes.

It is an apparent conundrum how plants evolved effector-triggered immunity (ETI), involving programmed cell death (PCD), as a major defence mechanism against biotrophic pathogens, because ETI-associated PCD could leave them vulnerable to necrotrophic pathogens that thrive on dead host cells. Interestingly, during ETI, the normally antagonistic defence hormones, salicylic acid (SA) and jasmonic acid (JA) associated with defence against biotrophs and necrotrophs respectively, both accumulate to high levels. In this study, we made the surprising finding that JA is a positive regulator of RPS2-mediated ETI. Early induction of JA-responsive genes and de novo JA synthesis following SA accumulation is activated through the SA receptors NPR3 and NPR4, instead of the JA receptor COI1. We provide evidence that NPR3 and NPR4 may mediate this effect by promoting degradation of the JA transcriptional repressor JAZs. This unique interplay between SA and JA offers a possible explanation of how plants can mount defence against a biotrophic pathogen without becoming vulnerable to necrotrophic pathogens. Salicylic acid (SA) and jasmonic acid (JA) often act antagonistically in plant defence. Here, Liu et al . show that during effector-triggered immunity (ETI) against Pseudomonas syringae , JA signalling is activated via a non-canonical pathway involving the SA receptors, NPR3 and NPR4, to positively regulate ETI.

Environmental conditions profoundly affect plant disease development; however, the underlying molecular bases are not well understood. Here we show that elevated temperature significantly increases the susceptibility of Arabidopsis to Pseudomonas syringae pv. tomato ( Pst ) DC3000 independently of the phyB/PIF thermosensing pathway. Instead, elevated temperature promotes translocation of bacterial effector proteins into plant cells and causes a loss of ICS1-mediated salicylic acid (SA) biosynthesis. Global transcriptome analysis reveals a major temperature-sensitive node of SA signalling, impacting ~60% of benzothiadiazole (BTH)-regulated genes, including ICS1 and the canonical SA marker gene, PR1 . Remarkably, BTH can effectively protect Arabidopsis against Pst DC3000 infection at elevated temperature despite the lack of ICS1 and PR1 expression. Our results highlight the broad impact of a major climate condition on the enigmatic molecular interplay between temperature, SA defence and function of a central bacterial virulence system in the context of a widely studied susceptible plant–pathogen interaction. Temperature is known to influence plant disease development. Here Huot et al. show that elevated temperature can enhance Pseudomonas syringae effector delivery into plant cells and suppress SA biosynthesis while also finding a temperature-sensitive branch of the SA signaling pathway in Arabidopsis .

Plants are continuously threatened by pathogen attack and, as such, they have evolved mechanisms to evade, escape and defend themselves against pathogens. However, it is not known what types of defense mechanisms a plant would already possess to defend against a potential pathogen that has not co-evolved with the plant. We addressed this important question in a comprehensive manner by studying the responses of 1041 accessions of Arabidopsis thaliana to the foliar pathogen Pseudomonas syringae pv. tomato (Pst) DC3000. We characterized the interaction using a variety of established methods, including different inoculation techniques, bacterial mutant strains, and assays for the hypersensitive response, salicylic acid (SA) accumulation and reactive oxygen species production. Fourteen accessions showed resistance to infection by Pst DC3000. Of these, two accessions had a surface-based mechanism of resistance, six showed a hypersensitive-like response while three had elevated SA levels. Interestingly, A. thaliana was discovered to have a recognition system for the effector AvrPto, and HopAM1 was found to modulate Pst DC3000 resistance in two accessions. Our comprehensive study has significant implications for the understanding of natural disease resistance mechanisms at the species level and for the ecology and evolution of plant–pathogen interactions.

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.

A β-glucosidase gene (bglA) from Butyrivibrio fibrisolvens H17c was cloned into the binary vector pGA482 under the control of the 35S Cauliflower Mosaic Virus (CaMV) promoter. A second construct was generated for accumulation of the bglA gene product in the vacuole of transformed tobacco plants. Reverse transcription - polymerase chain reaction analysis demonstrated that the bglA gene was expressed in 71% of cytosol-targeted and 67% of vacuole-targeted transgenic tobacco T₁ plants. T₁ transgenic plants (pGLU100 and pGLU200) exhibited elevated levels of free salicylic acid (SA) with a concomitant significant decrease in the level of glucosylsalicylic acid (GSA) compared to the untransformed tobacco plants and tobacco plants transformed with the empty vector (pGA482). Following inoculation with Tobacco Mosaic Virus (TMV), lesion area was 51% smaller in pGLU100 plants and 60% smaller in pGLU200 plants compared to inoculated untransformed and negative control plants.