Temperature‐dependent autoimmunity mediated by chs1 requires its neighboring TNL gene SOC3

Abstract

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 CHS1 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 SOC3, which is adjacent to CHS1 on chromosome 1. Expression of SOC3 was upregulated in the chs1-2 mutant. Mutations in six soc3 alleles and downregulation of SOC3 by an artificial microRNA construct fully rescued the chilling sensitivity and defense defects of chs1-2. Biochemical studies showed that CHS1 interacted with the NB and LRR domains of SOC3; however, mutated chs1 interacted with the TIR, NB and LRR domains of SOC3 in vitro and in vivo. This study reveals that the TN protein CHS1 interacts with the TNL protein SOC3 to modulate temperature-dependent autoimmunity.

E3 ligase SAUL1 serves as a positive regulator of PAMP‐triggered immunity and its homeostasis is monitored by immune receptor SOC3

“…To further confirm the proper identification of SOC3 , we obtained two exonic T‐DNA knockout alleles of soc3 , SALK_200339 designated as soc3‐21 , and SALK_069931 previously designated as soc3‐7 (Fig. b,c) (Zhang et al ., ). The saul1‐1 soc3‐21 double mutant completely reverted saul1 to WT morphology (Fig.…”

“…Zhang et al . () detected a direct interaction between SOC3 and CHS1. CHS1 could thus be such a candidate intermediate in regulating the activity of SOC3.…”

“…From two independent saul1 suppressor screens conducted in Canada and Germany, we identified many alleles of the saul1 suppressor susa1 . Interestingly, SUSA1 encodes a TNL protein, named SOC3 (Zhang et al ., ), which is able to interact with SAUL1 in planta . The autoimmune responses of both knockout and overexpression of SAUL1 rely on SOC3.…”

TIR-only protein RBA1 recognizes a pathogen effector to regulate cell death inArabidopsis

“…There is also precedence for TIR-NB proteins regulating full-length TNLs. The chs1-2 (a TIR-NB) mutant phenotype of temperature-dependent cell death requires the neighboring full-length TNL gene SOC1 (54). Truncated NLR proteins also have been reported to arise from a single full-length TNL gene via alternative splicing (55,56).…”

TIR‐NB‐LRR immune receptor SOC3 pairs with truncated TIR‐NB protein CHS1 or TN2 to monitor the homeostasis of E3 ligase SAUL1

“…However, the head‐to‐head arrangement of SOC3 , CHS1 and TN2 on chromosome 1 resembles that of previously reported paired NLR genes such as RPS4‐RRS1 and RGA4‐RGA5 (Cesari et al ., ; Saucet et al ., ). In addition, both loss‐of‐function alleles of SOC3 and CHS1 were identified from a suppressor screen using a gain‐of‐function mutant chs1‐2 , and SOC3 and CHS1 associate with each other i n planta (Zhang et al ., ). These observations prompted us to test whether CHS1 and TN2 could redundantly pair with SOC3 in saul1 ‐mediated autoimmunity.…”