Distinct mechanisms of plant immune resilience revealed by natural variation in warm temperature-modulated disease resistance amongArabidopsisaccessions

Abstract

AbstractElevated temperature suppresses production of the key plant defence hormone salicylic acid (SA). Heat-mediated SA suppression and resulting plant vulnerability are due to downregulated expression ofCALMODULIN BINDING PROTEIN 60-LIKE G(CBP60g) andSYSTEMIC ACQUIRED RESISTANCE DEFICIENT 1(SARD1), which encode master regulators of plant immunity. However, previous studies inArabidopsis thalianaplants have primarily focused on the accession Columbia-0 (Col-0), while the mechanisms governing the intraspecific variation inArabidopsisimmunity under elevated temperature have remained unknown. Here we show that BASIC HELIX LOOP HELIX 059 (bHLH059), a thermosensitive SA regulator at non-stress temperatures, does not regulate immune suppression under warmer temperatures. In agreement, temperature-resilient and -sensitiveArabidopsisaccessions based on disease resistance to the bacterial pathogenPseudomonas syringaepv.tomato(Pst) DC3000 did not correlate withbHLH059sequence polymorphisms. Instead, we found that different temperature-resilient accessions exhibit varyingCBP60gandSARD1expression profiles, potentially revealing bothCBP60g/SARD1-dependent and independent mechanisms of plant immune resilience to warming temperature. Collectively, this study has unveiled the intraspecific diversity ofArabidopsisimmune responses under warm temperatures. Our dissection of mechanisms underlying temperature-modulated plant immunity could aid in predicting plant responses to climate change and provide foundational knowledge for climate-resilient crop engineering.