WRKY8 transcription factor functions in the TMV-cg defense response by mediating both abscisic acid and ethylene signaling in Arabidopsis
WRKY8 transcription factor functions in the TMV-cg defense response by mediating both abscisic acid and ethylene signaling in Arabidopsis
复制标题
WRKY8 转录因子通过介导拟南芥中的脱落酸和乙烯信号传导在 TMV-cg 防御反应中发挥作用
DOI：
10.1073/pnas.1221347110
复制
发表时间：
2013-05-21
影响因子：
11.1
通讯作者：
Yu, Diqiu
中科院分区：
文献类型：
--
作者：
Chen, Ligang;Zhang, Liping;Yu, Diqiu
WRKY转录因子是植物免疫反应中的关键因子，但人们对它们参与抗病毒防御的了解较少，更多的是了解它们在抵御细菌或真菌病原体方面的作用。在这里，我们报道了拟南芥WRKY DNA结合蛋白8(WRKY8)在介导侵染十字花科植物的烟草花叶病毒(TMV-CG)的长距离移动中的作用。WRKY8的表达受到TMV-CG侵染的抑制，而WRKY8的突变加速了TMV-CG在系统感染叶片中的积累。定量RT-PCR分析表明，在系统感染的WRKY8叶片中，ABA不敏感4(ABI4)的表达降低，1-氨基环丙烷-1-羧酸合成酶6(ACS6)和乙烯反应因子104(ERF104)的表达增强。免疫沉淀实验表明，WRKY8可以选择性地与ABI4、ACS6和ERF104启动子的W盒结合。此外，TMV-CG感染增强了WRKY8与ABI4启动子的结合，但降低了WRKY8与ACS6和ERF104启动子的结合，表明WRKY8对ABI4、ACS6和ERF104的调控至少部分依赖于TMV-CG。外源脱落酸(ABA)减少了TMV-CG的系统积累。ABA缺陷1、ABA缺陷2、ABA缺陷3或abi4突变加速了系统TMV-CG的积累。相反，外源应用氨基环丙烷-1-羧酸促进了TMV-CG的系统积累，但acs6、erf104或一个八重ACS突变体的突变抑制了系统TMV-CG的积累。我们的结果表明，WRKY8通过直接调控ABI4、ACS6和ERF104的表达参与了对TMV-CG的防御反应，并可能在TMV-CG-拟南芥互作过程中介导了ABA和乙烯信号之间的串扰。
WRKY transcription factors are key players in the plant immune response, but less is known about their involvement in antiviral defense than about their roles in defense against bacterial or fungi pathogens. Here, we report that Arabidopsis thaliana WRKY DNA-binding protein 8 (WRKY8) has a role in mediating the long-distance movement of crucifer-infecting tobacco mosaic virus (TMV-cg). The expression of WRKY8 was inhibited by TMV-cg infection, and mutation of WRKY8 accelerated the accumulation of TMV-cg in systemically infected leaves. Quantitative RT-PCR analysis showed that the expression of ABA insensitive 4 (ABI4) was reduced and the expression of 1-aminocyclopropane-1-carboxylic acid synthase 6 (ACS6) and ethylene response factor 104 (ERF104) was enhanced in the systemically infected leaves of wrky8. Immunoprecipitation assays demonstrated that WRKY8 could bind selectively to putative W-boxes of the ABI4, ACS6, and ERF104 promoters. Furthermore, TMV-cg infection enhanced WRKY8 binding to the ABI4 promoter but reduced the binding of WRKY8 to the ACS6 and ERF104 promoters, indicating that regulation of ABI4, ACS6, and ERF104 by WRKY8 is at least partially dependent on TMV-cg. Exogenous applications of abscisic acid (ABA) reduced the systemic accumulation of TMV-cg. Mutations in ABA deficient 1, ABA deficient 2, ABA deficient 3, or abi4 accelerated systemic TMV-cg accumulation. In contrast, exogenous application of aminocyclopropane-1-carboxylic acid enhanced the systemic accumulation of TMV-cg, but mutations in acs6, erf104, or an octuple acs mutant inhibited systemic TMV-cg accumulation. Our results demonstrate that WRKY8 is involved in the defense response against TMV-cg through the direct regulation of the expression of ABI4, ACS6, and ERF104 and may mediate the crosstalk between ABA and ethylene signaling during the TMV-cg-Arabidopsis interaction.