An elevated growth temperature often inhibits plant defense responses and renders plants more susceptible to pathogens. However, the molecular mechanisms underlying this modulation are unknown. To genetically dissect this regulation, we isolated mutants that retain disease resistance at a higher growth temperature in Arabidopsis. One such heat-stable mutant results from a point mutation in SNC1, a NB-LRR encoding gene similar to disease resistance (R) genes. Similar mutations introduced into a tobacco R gene, N, confer defense responses at elevated temperature. Thus R genes or R-like genes involved in recognition of pathogen effectors are likely the causal temperature-sensitive component in defense responses. This is further supported by snc1 intragenic suppressors that regained temperature sensitivity in defense responses. In addition, the SNC1 and N proteins had a reduction of nuclear accumulation at elevated temperature, which likely contributes to the inhibition of defense responses. These findings identify a plant temperature sensitive component in disease resistance and provide a potential means to generate plants adapting to a broader temperature range. It has been known that temperature modulates plant immune responses, but the molecular mechanisms underlying this modulation are unknown. Our study describes a novel finding that the NB-LRR type of R or R-like protein is the temperature-sensitive component of plant defense responses. R or R-like proteins have ‘receptor’ like functions involved in specific recognition of pathogens. Through genetic screens and targeted mutagenesis, we found that alterations in the R-like gene SNC1 and the R gene N can change temperature sensitivity of defense responses. Further, an elevated temperature reduced the nuclear accumulation of SNC1, which likely contributes to the inhibition of disease resistance at high temperatures. Our study indicates that NB-LRR proteins mediate temperature sensitivity in plant immune responses.

Plant growth homeostasis and defense responses are regulated by BONZAI1 (BON1), an evolutionarily conserved gene. Here, we show that growth regulation by BON1 is mediated through defense responses. BON1 is a negative regulator of a haplotype-specific Resistance (R) gene SNC1. The bon1-1 loss-of-function mutation activates SNC1, leading to constitutive defense responses and, consequently, reduced cell growth. In addition, a feedback amplification of the SNC1 gene involving salicylic acid is subject to temperature control, accounting for the regulation of growth and defense by temperature in bon1-1 and many other mutants. Thus, plant growth homeostasis involves the regulation of an R gene by BON1 and the intricate interplay between defense responses and temperature responses.

Plant-pathogen interactions are known to be affected by environmental factors including temperature; however, the temperature effects have not been systematically studied in plant disease resistance. Here, we characterized the effects of a moderate increase in temperature on resistance to bacterial pathogen Pseudomonas syringae and two viral elicitors in Arabidopsis thaliana and Nicotiana benthamiana. Both the basal and the resistance (R) gene–mediated defense responses to Pseudomonas syringae are found to be inhibited by a moderately high temperature, and hypersensitive responses induced by R genes against two viruses are also reduced by an increase of temperature. These indicate that temperature modulation of defense responses to biotrophic and hemibiotrophic pathogens might be a general phenomenon. We further investigated the roles of two small signaling molecules, salicylic acid and jasmonic acid, as well as two defense regulators, EDS1 and PAD4, in this temperature modulation. These components, though modulated by temperature or involved in temperature regulation or both, are not themselves determinants of temperature sensitivity in the defense responses analyzed. The inhibition of plant defense response by a moderately high temperature may thus be mediated by other defense signaling components or a combination of multiple factors.

Cyclic nucleotide-gated ion channels in rice promote tolerance to both heat and chilling and affect the calcium response to temperature stresses.