Temperature‐dependent autoimmunity mediated by chs1 requires its neighboring TNL gene SOC 3

Summary Toll/interleukin receptor ( TIR )‐nucleotide binding site ( NB )‐type ( TN ) proteins are encoded by a family of 21 genes in the Arabidopsis genome. Previous studies have shown that a mutation in the TN gene CHS 1 activates the activation of defense responses at low temperatures. However, the underlying molecular mechanism remains unknown. To genetically dissect chs1‐mediated signaling, we isolated genetic suppressors of chs1‐2 ( soc ). Several independent soc mutants carried mutations in the same TIR ‐ NB ‐leucine‐rich repeat ( LRR ) ( TNL )‐encoding gene SOC 3, which is adjacent to CHS 1 on chromosome 1. Expression of SOC 3 was upregulated in the chs1‐2 mutant. Mutations in six soc3 alleles and downregulation of SOC 3 by an artificial micro RNA construct fully rescued the chilling sensitivity and defense defects of chs1‐2 . Biochemical studies showed that CHS 1 interacted with the NB and LRR domains of SOC 3; however, mutated chs1 interacted with the TIR , NB and LRR domains of SOC 3 in vitro and in vivo . This study reveals that the TN protein CHS 1 interacts with the TNL protein SOC 3 to modulate temperature‐dependent autoimmunity.