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

文献类型： 外文期刊

第一作者： Zhang, Yao

作者： Zhang, Yao;Wang, Yuancong;Liu, Jingyan;Ding, Yanglin;Zhang, Xiaoyan;Yang, Shuhua;Wang, Yuancong;Wang, Shanshan;Liu, Yule;Wang, Shanshan;Liu, Yule

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关键词： Arabidopsis;autoimmunity;chilling stress;CHS1;TIR-NB protein;TIR-NB-LRR protein

期刊名称：NEW PHYTOLOGIST （ 影响因子：10.151； 五年影响因子：10.475 ）

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收录情况： SCI

摘要： 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 invitro and invivo. This study reveals that the TN protein CHS1 interacts with the TNL protein SOC3 to modulate temperature-dependent autoimmunity.

分类号： Q94

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