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Biology subjects

Demont, H.

Publications and source records attributed to Demont, H..

2 recordsLinked to original sources

Natural variation in an NLR pair confers thermostable resistance to a devastating bacterial pathogen

Climate change reshapes host-pathogen interactions by increasing pathogen aggressiveness and weakening plant immune responses, particularly under heat stress. Nucleotide-binding leucine-rich repeat (NLR) immune receptors, key players in pathogen recognition, are altered under elevated temperatures in both plants and mammals, posing a major challenge to disease resistance. In Arabidopsis thaliana, the well-described RPS4/RRS1 NLR pair confers resistance to the worldwide devastating phytopathogenic Ralstonia pseudosolanacearum. Here, by combining the exploration of natural genetic variation with genetic mapping, polymorphism analysis, structural modeling, and functional complementation, we demonstrated that the paucity of full thermostable resistance is primarily associated with a unique RPS4/RRS1 haplotype carrying key substitutions in leucine-rich repeat domains. These findings reveal natural genetic diversity as a source of thermostable resistance, highlighting promising opportunities to engineer climate-resilient plants.

plant biology↗

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

Plant disease is a major threat in agriculture and climate change is predicted to intensify it. Above the optimal plants 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{degrees}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.

plant biology↗