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Calcium (Ca2+) signalling regulates salicylic acid (SA)‐mediated immune response through calmodulin‐meditated transcriptional activators, AtSRs/CAMTAs, but its mechanism is not fully understood. Here, we report an AtSR1/CAMTA3‐mediated regulatory mechanism involving the expression of the SA receptor, NPR1. Results indicate that the transcriptional expression of NPR1 was regulated by AtSR1 binding to a CGCG box in the NPR1 promotor. The atsr1 mutant exhibited resistance to the virulent strain of Pseudomonas syringae pv. tomato (Pst), however, was susceptible to an avirulent Pst strain carrying avrRpt2, due to the failure of the induction of hypersensitive responses. These resistant/susceptible phenotypes in the atsr1 mutant were reversed in the npr1 mutant background, suggesting that AtSR1 regulates NPR1 as a downstream target during plant immune response. The virulent Pst strain triggered a transient elevation in intracellular Ca2+ concentration, whereas the avirulent Pst strain triggered a prolonged change. The distinct Ca2+ signatures were decoded into the regulation of NPR1 expression through AtSR1's IQ motif binding with Ca2+‐free‐CaM2, while AtSR1's calmodulin‐binding domain with Ca2+‐bound‐CaM2. These observations reveal a role for AtSR1 as a Ca2+‐mediated transcription regulator in controlling the NPR1‐mediated plant immune response. Calcium signalling regulates salicylic acid (SA)‐mediated immune response through calmodulin‐meditated transcriptional activators, AtSRs/CAMTAs, but its mechanism is not clearly understood. Here, we report an AtSR1/CAMTA3‐mediated regulatory mechanism involving the expression of the SA receptor, NPR1. These observations reveal an additional mechanism for controlling the NPR1‐mediated plant immune response. A better understanding of plant immunity should help in modern agriculture. Hence, this topic is of major interest to plant scientists. The Arabidopsis thaliana lines used in this study are wild‐type (WT) Columbia (Col‐0) and loss‐of‐function atsr1 mutant (Salk_001152C). [ABSTRACT FROM AUTHOR]

Changing temperatures are known to affect plant–microbe interactions; however, the molecular mechanism involved in plant disease resistance is not well understood. Here, we report the effects of a moderate change in temperature on plant immune response through Ca2+/calmodulin-mediated signaling. At 30 °C, Pst DC3000 triggered significantly weak and relatively slow Ca2+ influx in plant cells, as compared to that at 18 °C. Increased temperature contributed to an enhanced disease susceptibility in plants; the enhanced disease susceptibility is the result of the compromised stomatal closure induced by pathogens at high temperature. A Ca2+ receptor, AtSR1, contributes to the decreased plant immunity at high temperatures and the calmodulin-binding domain (CaMBD) is required for its function. Furthermore, both salicylic acid biosynthesis (ICS) and salicylic acid receptor (NPR1) are involved in this process. In addition to stomatal control, AtSR1 is involved in high temperature-compromised apoplastic immune response through the salicylic acid signaling pathway. The qRT-PCR data revealed that AtSR1 contributed to increased temperatures-mediated susceptible immune response by regulating SA-related genes in atsr1, such as PR1, ICS1, NPR1, as well as EDS1. Our results indicate that Ca2+ signaling has broad effects on the molecular interplay between changing temperatures as well as plant defense during plant–pathogen interactions. [ABSTRACT FROM AUTHOR]