Temperature-dependentautoimmunity mediated by chs1 requires its neighboring TNL gene SOC3
Temperature-dependentautoimmunity mediated by chs1 requires its neighboring TNL gene SOC3
复制标题
chs1介导的温度依赖性自身免疫需要其邻近的TNL基因SOC3
DOI：
10.1111/nph.14216
复制
发表时间：
2017
期刊：
影响因子：
9.4
通讯作者：
Shuhua Yang
中科院分区：
文献类型：
--
作者：
Yao Zhang;Yuancong Wang;Jingyan Liu;Yanglin Ding;Shanshan Wang;Xiaoyan Zhang;Yule Liu;Shuhua Yang
Toll/白细胞介素型受体(TIR)-核苷酸结合位点(Nb)型(TN)蛋白是由拟南芥基因组中的21个基因组成的家族编码的。先前的研究表明，在低温下，TN基因CHS1的突变会激活防御反应。然而，潜在的分子机制仍不清楚。为了从基因上剖析chs1介导的信号转导，我们分离了chs1-2的遗传抑制因子(Soc)。与CHS1相邻的TIR-NB-亮氨酸重复序列(TnL)编码基因SOC3在几个独立突变株中均有突变，突变株1-2上调了SOC3的表达。6个等位基因的突变和人工microRNA构建的SOC3的下调完全挽救了chs1-2的冷敏和防御缺陷。生化研究表明，chs1与SOC3的NB和LRR结构域相互作用，而突变的chs1在体外与SOC3的TIR、NB和LRR结构域相互作用。本研究揭示了TN蛋白CHS1与TNL蛋白SOC3相互作用调节温度依赖性自身免疫。
Toll/interleukin receptor (TIR)‐nucleotide binding site (NB)‐type (TN) proteins are encoded by a family of 21 genes in theArabidopsisgenome. Previous studies have shown that a mutation in theTNgeneCHS1activates 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 ofchs1‐2(soc). Several independentsocmutants carried mutations in the same TIR‐NB‐leucine‐rich repeat (LRR) (TNL)‐encoding geneSOC3,which is adjacent toCHS1on chromosome 1.Expression ofSOC3was upregulated in thechs1‐2mutant. Mutations in sixsoc3alleles and downregulation ofSOC3by an artificial microRNA construct fully rescued the chilling sensitivity and defense defects ofchs1‐2. 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 SOC3in vitroandin vivo.This study reveals that the TN protein CHS1 interacts with the TNL protein SOC3 to modulate temperature‐dependent autoimmunity.