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.