IRE1 regulated autophagy and chaperone levels cooperatively modulate acquired thermotolerance inArabidopsis thaliana

Abstract

AbstractRapidly changing global climatic conditions emphasize the urgent need for the development of heat stress-resilient plants. Priming, a stress-training program that aids in imparting tolerance to subsequent stress(es) emerged as a promising approach to improve stress tolerance. However, molecular mechanisms underlying priming-induced plant stress responses still remain largely elusive. In the current study, the impact of heat stress onArabidopsis thalianaseedlings pre-exposed to elevated temperature (primed) was found to be minimal, compared to naïve (unprimed) seedlings, which failed to survive. Our findings suggest that thermopriming-mediated heat stress tolerance operates through the activation of IRE1-bZIP60 cascade triggering unfolded protein response (UPR). Further, IRE1 activation triggers autophagy response through attenuation of autophagy-negative regulators such asBGLU21, ROSY1andPR-14via RIDD-mediated mRNA degradation. Alongside UPR and autophagy, priming temporally induces HSP levels, rendering plants tolerant to acute heat stress. Contrarily, unprimed seedlings fail to mount such temporally coordinated regulation, thus fail to survive. Moreover, loss of bZIP60 reduces the impact of priming-induced response, suggesting its role in the maintenance of stress memory. Taken together, the current study suggests that priming-mediated regulation of protein homeostasis through the temporal regulation of autophagy in concert with chaperone synthesis promotes heat stress tolerance.