TCP Transcription Factors Interact With NPR1 and Contribute Redundantly to Systemic Acquired Resistance.
TCP Transcription Factors Interact With NPR1 and Contribute Redundantly to Systemic Acquired Resistance.
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DOI：
10.3389/fpls.2018.01153
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发表时间：
2018
影响因子：
5.6
通讯作者：
Fu ZQ
中科院分区：
文献类型：
--
作者：
Li M;Chen H;Chen J;Chang M;Palmer IA;Gassmann W;Liu F;Fu ZQ
在拟南芥中，TEOSINTE BRANCHED 1、CYCLOIDEA、PCF 1（TCP）转录因子（TF）在发育过程中起着重要作用。最近的研究表明，它们也在植物免疫中发挥作用，但它们是否在系统获得性抗性（SAR）中发挥重要作用仍不清楚。PR基因非表达子1（NPR 1）作为SAR中一个重要的转录调控节点，通过与转录因子相互作用对下游基因表达起调控作用。在这项工作中，我们提供的生化和遗传证据表明，TCP 8，TCP 14和TCP 15参与SAR信号通路。在酵母双杂交试验中，TCP 8、TCP 14和TCP 15与NPR 1发生物理相互作用，这些相互作用在体内得到了进一步证实。SAR对假单胞菌致病变种（Pseudomonaseryningae pv.）与哥伦比亚0（Col-0）野生型植物相比，在三重T-DNA插入突变体tcp 8 -1 tcp 14 -5 tcp 15 -3中的斑点霉（Psm）ES 4326部分受损。与Col-0相比，在用携带avrRpt 2的Psm ES 4326局部处理后，在tcp 8 -1 tcp 14 -5 tcp 15 -3突变体中局部和系统叶片中SAR标记基因PR 1、PR 2和PR 5的诱导显著降低。酵母单杂交和染色质免疫沉淀（ChIP）试验的结果表明，TCP 15可以结合到一个保守的TCP结合基序，GCGGGAC，在PR 5的启动子，这种结合被NPR 1增强。来自RT-qPCR测定的结果显示，TCP 15响应于水杨酸诱导而促进PR 5的表达。综上所述，这些数据揭示了TCP 8、TCP 14和TCP 15与NPR 1物理相互作用并冗余地发挥功能以建立SAR，TCP 15通过直接结合PR 5启动子内的TCP结合位点促进PR 5的表达，并且这种结合被NPR 1增强。
In Arabidopsis, TEOSINTE BRANCHED 1, CYCLOIDEA, PCF1 (TCP) transcription factors (TF) play critical functions in developmental processes. Recent studies suggest they also function in plant immunity, but whether they play an important role in systemic acquired resistance (SAR) is still unknown. NON-EXPRESSER OF PR GENES 1 (NPR1), as an essential transcriptional regulatory node in SAR, exerts its regulatory role in downstream genes expression through interaction with TFs. In this work, we provide biochemical and genetic evidence that TCP8, TCP14, and TCP15 are involved in the SAR signaling pathway. TCP8, TCP14, and TCP15 physically interacted with NPR1 in yeast two-hybrid assays, and these interactions were further confirmed in vivo. SAR against the infection of virulent strain Pseudomonas syringae pv. maculicola (Psm) ES4326 in the triple T-DNA insertion mutant tcp8-1 tcp14-5 tcp15-3 was partially compromised compared with Columbia 0 (Col-0) wild type plants. The induction of SAR marker genes PR1, PR2, and PR5 in local and systemic leaves was dramatically decreased in the tcp8-1 tcp14-5 tcp15-3 mutant compared with that in Col-0 after local treatment with Psm ES4326 carrying avrRpt2. Results from yeast one-hybrid and chromatin immunoprecipitation (ChIP) assays demonstrated that TCP15 can bind to a conserved TCP binding motif, GCGGGAC, within the promoter of PR5, and this binding was enhanced by NPR1. Results from RT-qPCR assays showed that TCP15 promotes the expression of PR5 in response to salicylic acid induction. Taken together, these data reveal that TCP8, TCP14, and TCP15 physically interact with NPR1 and function redundantly to establish SAR, that TCP15 promotes the expression of PR5 through directly binding a TCP binding site within the promoter of PR5, and that this binding is enhanced by NPR1.
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