TNL ‐mediated immunity in A rabidopsis requires complex regulation of the redundant ADR 1 gene family

Summary Nucleotide‐binding leucine‐rich repeat proteins ( NLR s) serve as intracellular immune receptors in animals and plants. Sensor NLR s perceive pathogen‐derived effector molecules and trigger robust host defense. Recent studies revealed the role of three coiled‐coil‐type NLR s ( CNL s) of the ADR 1 family – ADR 1, ADR 1‐L1 and ADR 1‐L2 – as redundant helper NLR s, whose function is required for defense mediated by multiple sensor NLR s. From a mutant snc1 ‐enhancing ( MUSE ) forward genetic screen in A rabidopsis targeted to identify negative regulators of snc1 that encodes a TIR ‐type NLR ( TNL ), we isolated two alleles of muse15 , both carrying mutations in ADR 1‐L1 . Interestingly, loss of ADR 1‐L1 also enhances immunity‐related phenotypes in other autoimmune mutants including cpr1 , bal and lsd1 . This immunity‐enhancing effect is not mediated by increased SNC 1 protein stability, nor is it fully dependent on the accumulation of the defense hormone salicylic acid ( SA ). Transcriptional analysis revealed an upregulation of ADR 1 and ADR 1‐L2 in the adr1‐L1 background, which may overcompensate the loss of ADR 1‐L1 , resulting in enhanced immunity. Interestingly, autoimmunity of snc1 and chs2 , which encode typical TNL s, is fully suppressed by the adr1 triple mutant, suggesting that the ADR s are required for TNL downstream signaling. This study extends our knowledge on the interplay among ADR s and reveals their complexity in defense regulation.