P-027 - Determination of the functional redundancy and p-loop dependency of Arabidopsis RNLs

Many plant cell surface receptors-pattern-recognition-receptors (PRRs) and intracellular immune receptors- leucine-rich repeat receptors (NLRs) are mediated downstream signalling cascades for  immune activation. The initiation sensor NLR-dependent autoimmunity depends on the presence of members of a certain NLR subfamily, termed “helper”- hNLRs or RNLs. In Arabidopsis thaliana, RNLs are encoded by two gene families, ADR1 and NRG1. Recent research demonstrated that the two RNL subfamilies function in an unequal redundant manner and showed that at least some RNL functions are non-canonical, meaning they do not require a functional P-loop motif important for nucleotide binding. We aim to understand to what extend the ADR1s and NRG1s are redundantly acting in immunity inside the two subfamilies and whether all RNL helper functions are P-loop independent. Based on our results, we suggest that the individual members of the two subfamilies are also unequally redundant in mediating immunity inside the two subfamilies. Interestingly, all RNL P-loop mutants did complement tested RNL combinatorial mutants in a similar manner as the wild-type proteins – thus, indicating that all tested hNLR functions in Arabidopsis are p-loop independent. This is particularly interesting, since a functional P-loop was previously shown to be required for proper cell-death induction by RNLs. We are currently examining how these P-loop mutants mechanistically induce immunity in Arabidopsis.