Pepper CabZIP63 acts as a positive regulator during Ralstonia solanacearum or high temperature-high humidity challenge in a positive feedback loop with CaWRKY40.
Pepper CabZIP63 acts as a positive regulator during Ralstonia solanacearum or high temperature-high humidity challenge in a positive feedback loop with CaWRKY40.
复制标题
Pepper CabZIP63 在与 CaWRKY40 的正反馈回路中，在青枯菌或高温高湿挑战期间充当正调节剂
DOI：
10.1093/jxb/erw069
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发表时间：
2016-04
影响因子：
6.9
通讯作者：
He S
中科院分区：
文献类型：
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作者：
Shen L;Liu Z;Yang S;Yang T;Liang J;Wen J;Liu Y;Li J;Shi L;Tang Q;Shi W;Hu J;Liu C;Zhang Y;Lin W;Wang R;Yu H;Mou S;Hussain A;Cheng W;Cai H;He L;Guan D;Wu Y;He S
CaWRKY40间接激活的CabZIP63正向调控了CabZIP63和CaWRKY40的转录，增强了CaWRKY40与其目标启动子的结合，从而提高了对青枯病的抗性和耐热性。已知CaWRKY40在辣椒(Capsicum Annuum)对接种青枯雷尔氏菌(RSI)或高温高湿(HTHH)的反应中起到正向调节作用，但其潜在机制仍不清楚。在此，我们报道了辣椒bZIP家族成员CabZIP63通过调控CaWRKY40的表达参与了这一过程。研究发现，CabZIP63定位于细胞核内，可被RSI或HTHH上调，可与CabZIP63(PCabZIP63)和CaWRKY40(PCaWRKY40)启动子结合，并以C盒或G盒依赖的方式激活由pCabZIP63和pCaWRKY40驱动的β-葡萄糖醛酸苷酶的表达。通过病毒诱导的基因沉默(VIGS)在辣椒植株中沉默CabZIP63，显著降低了辣椒对RSI的抗性和对HTHH的耐性，同时下调了免疫或耐热相关的CaPR1、CaNPR1、CaDEF1和CaHSP24。瞬时过表达(TOE)可诱导过敏性反应诱导的细胞死亡和免疫和耐热相关标记基因的表达，但可被CabZIP63-SRDX所抑制。此外，CaZIP63与pCaWRKY40的结合可被RSI或HTHH上调，CaWRKY40的转录水平以及CaWRKY40与CaPR1、CaNPR1、CaDEF1和CaHSP24启动子的结合可被CAZIP63的TOE上调。另一方面，CaWRKY40的TOE也上调了CabZIP63的转录水平。这些数据表明，CabZIP63直接或间接地在转录和转录后水平调控CaWRKY40的表达，在辣椒对RSI或HTHH的反应中与CaWRKY40形成正反馈环。综上所述，我们的数据将有助于阐明辣椒对RSI和HTHH的反应之间串扰的潜在机制。
CabZIP63, indirectly activated by CaWRKY40, positively modulates transcription of CabZIP63 and CaWRKY40, enhances the binding of CaWRKY40 to its target promoters, and, therefore, increases resistance to Ralstonia solanacearum and thermotolerance. CaWRKY40 is known to act as a positive regulator in the response of pepper (Capsicum annuum) to Ralstonia solanacearum inoculation (RSI) or high temperature–high humidity (HTHH), but the underlying mechanism remains elusive. Herein, we report that CabZIP63, a pepper bZIP family member, participates in this process by regulating the expression of CaWRKY40. CabZIP63 was found to localize in the nuclei, be up-regulated by RSI or HTHH, bind to promoters of both CabZIP63 (pCabZIP63) and CaWRKY40 (pCaWRKY40), and activate pCabZIP63- and pCaWRKY40-driven β-glucuronidase expression in a C- or G-box-dependent manner. Silencing of CabZIP63 by virus-induced gene silencing (VIGS) in pepper plants significantly attenuated their resistance to RSI and tolerance to HTHH, accompanied by down-regulation of immunity- or thermotolerance-associated CaPR1, CaNPR1, CaDEF1, and CaHSP24. Hypersensitive response-mediated cell death and expression of the tested immunity- and thermotolerance-associated marker genes were induced by transient overexpression (TOE) of CabZIP63, but decreased by that of CabZIP63-SRDX. Additionally, binding of CabZIP63 to pCaWRKY40 was up-regulated by RSI or HTHH, and the transcript level of CaWRKY40 and binding of CaWRKY40 to the promoters of CaPR1, CaNPR1, CaDEF1 and CaHSP24 were up-regulated by TOE of CabZIP63. On the other hand, CabZIP63 was also up-regulated transcriptionally by TOE of CaWRKY40. The data suggest collectively that CabZIP63 directly or indirectly regulates the expression of CaWRKY40 at both the transcriptional and post-transcriptional level, forming a positive feedback loop with CaWRKY40 during pepper’s response to RSI or HTHH. Altogether, our data will help to elucidate the underlying mechanism of crosstalk between pepper’s response to RSI and HTHH.