Elevated temperatures a few degrees above the average will occur more often in the coming decades, posing a unique threat to plant’s survival that evolved for cooler temperatures. Temperature influences many elements of a plant’s immune system, which has been increasingly under threat as pathogens expand their range. Previous research has highlighted that the plant defense hormone salicylic acid is disrupted at elevated temperature in numerous plant species in response to pathogens. Research in Arabidopsis thaliana has identified molecular mechanisms contributing towards compromised SA biosynthesis and signaling which enhances their susceptibility to the bacterial pathogen Pseudomonas syringae pathovar. tomato DC3000. Understanding how elevated temperature compromises SA biosynthesis and signaling will be key for developing solutions to enable plants to have robust temperature tolerance and survive pathogens.In this dissertation, I will highlight how plants respond to elevated temperature and pathogen infection and examine the cross-section of this interaction through understanding plant stress hormones and how they interact with the immune system. Secondly, this thesis highlights research underpinning: 1). How elevated temperature interferes with upstream signaling elements of pathogen perception mechanisms that contribute towards SA biosynthesis and 2) How does supplementing exogenous SA in the form of benzothiadiazole (BTH) maintains plant immunity at elevated temperature despite the loss of canonical signaling like gene expression of PATHOGENESIS RELATED1 (PR1). This research is explored through the lens of the Arabidopsis thaliana – Pseudomonas syringae pv. tomato DC3000 plant-pathosystem. This study revealed that Pattern Triggered Immunity (PTI), the upstream plant perception mechanism that perceives conserved epitopes of pathogens, is weakened by elevated temperature. By using flg22, a pathogen derived conserved peptide, I identified that [Ca2+] flux and signaling are compromised at elevated temperature, and several defense outputs appear compromised that depend on [Ca2+] signaling. Salicylic acid has putatively been linked to [Ca2+]-dynamics and this thesis investigates how temperature modulation of [Ca2+] would interfere with SA biosynthesis and signaling. Furthermore, this study identified that the [Ca2+]-independent branch of immunity remains robust across the temperature range in this study. By investigating this temperature insensitive immune-signaling pathway, I revealed that their immune outputs can be enhanced at elevated temperature in response to BTH. This provides a novel framework for identifying how exogenous SA can prime a plant immune system in the absence of canonical signaling responses.
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