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Temperature‐dependent autoimmunity mediated by chs1 requires its neighboring TNL gene SOC 3
Author(s) -
Zhang Yao,
Wang Yuancong,
Liu Jingyan,
Ding Yanglin,
Wang Shanshan,
Zhang Xiaoyan,
Liu Yule,
Yang Shuhua
Publication year - 2017
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.14216
Subject(s) - mutant , gene , biology , downregulation and upregulation , genetics , mutation , microbiology and biotechnology
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.