Immune signaling induced by plant Toll/interleukin-1 receptor (TIR) domains is thermostable

Abstract

SummaryPlant disease is a major threat in agriculture and climate change is predicted to intensify it. Above the optimal plant’s growth range, plant immunity and in particular immune responses induced by nucleotide-binding leucine rich repeat receptors (NLRs) are dampened, but the underlying molecular mechanisms remains elusive. NLRs usually contain an N-terminal signaling domain, such as Toll/interleukin-1 receptor (TIR) domain, which is self-sufficient to trigger immune signaling. By using inducible Arabidopsis transgenic lines expressing TIR-containing NLRs (TNLs) or corresponding isolated TIR domains from Arabidopsis RPS4 and flax L6 NLRs, we showed that immune signaling induced downstream of TNL activation is not affected by an elevation of temperature. Conditional activation of TNL- and isolated TIR-mediated immune responses follow the same signaling route at permissive temperature (EDS1/RNLs requirement and activation of the salicylic acid sector). Yet, this signaling pathway is maintained under elevated temperature (30°C) when induced by isolated TIRs, but not full-length TNLs. This work underlines the need to further study how NLRs are impacted by an increase of temperature, which is particularly important to improve the resilience of plant disease resistance in a warming climate.