AIG2A and AIG2B limit the activation of salicylic acid-regulated defenses by tryptophan-derived secondary metabolism in Arabidopsis
AIG2A and AIG2B limit the activation of salicylic acid-regulated defenses by tryptophan-derived secondary metabolism in Arabidopsis
复制标题
AIG2A和AIG2B通过拟南芥中色氨酸衍生的次级代谢限制水杨酸调节的防御的激活
DOI：
10.1093/plcell/koac255
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Hua, Jian
中科院分区：
文献类型：
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作者：
Wang, Zhixue;Yang, Leiyun;Jander, Georg;Bhawal, Ruchika;Zhang, Sheng;Liu, Zhenhua;Oakley, Aaron;Hua, Jian
在拟南芥中，分别由一般的非自我信号和病原体信号诱导的含有拟南芥次生代谢产物（TDSMs）和水杨酸（SA）的化学防御系统。这些化学防御系统是否以及如何连接和平衡在很大程度上是未知的。在这项研究中，我们确定了AVRRPT 2诱导基因2A（AIG2A）和AIG2B基因作为防止TDSM激活SA防御系统的看门人。这些基因也被确定为抗病性CYP4A自然变异的重要贡献者。泰国自然加入。AIG2A和AIG2B功能的丧失导致SA和TDSM防御系统的上调。抑制筛选和遗传分析表明，在AIG2A和AIG2B的情况下，SA通路的上调需要功能性TDSM系统，但反之亦然。此外，AIG2A和AIG2B基因与TDSM生物合成基因通过一般病原体激发子和非自身信号共诱导，从而作为TDSM防御系统的反馈控制，以及限制TDSM对SA防御系统的激活。因此，这项研究揭示了AIG2A和AIG2B介导的机制，微调和平衡SA和TDSM化学防御系统，以应对非致病性和致病性微生物。
Chemical defense systems involving tryptophan-derived secondary metabolites (TDSMs) and salicylic acid (SA) are induced by general nonself signals and pathogen signals, respectively, inArabidopsis thaliana. Whether and how these chemical defense systems are connected and balanced is largely unknown. In this study, we identified theAVRRPT2-INDUCED GENE2A(AIG2A) andAIG2Bgenes as gatekeepers that prevent activation of SA defense systems by TDSMs. These genes also were identified as important contributors to natural variation in disease resistance amongA. thaliananatural accessions. The loss of AIG2A and AIG2B function leads to upregulation of both SA and TDSM defense systems. Suppressor screens and genetic analysis revealed that a functional TDSM system is required for the upregulation of the SA pathway in the absence of AIG2A and AIG2B, but not vice versa. Furthermore, theAIG2AandAIG2Bgenes are co-induced with TDSM biosynthesis genes by general pathogen elicitors and nonself signals, thereby functioning as a feedback control of the TDSM defense system, as well as limiting activation of the SA defense system by TDSMs. Thus, this study uncovers an AIG2A- and AIG2B-mediated mechanism that fine-tunes and balances SA and TDSM chemical defense systems in response to nonpathogenic and pathogenic microbes.