Suppression and activation of plant defense genes is comprehensively regulated by WRKY family transcription factors. Chickpea, the non-model crop legume suffers from wilt caused by Fusarium oxysporum f. sp. ciceri Race1 (Foc1), defense response mechanisms of which are poorly understood. Here, we attempted to show interaction between WRKY70 and several downstream signaling components involved in susceptibility/resistance response in chickpea upon challenge with Foc1. In the present study, we found Cicer arietinum L. WRKY70 (CaWRKY70) negatively governs multiple defense responsive pathways, including Systemic Acquired Resistance (SAR) activation in chickpea upon Foc1 infection. CaWRKY70 is found to be significantly accumulated at shoot tissues of susceptible (JG62) chickpea under Foc1 stress and salicylic acid (SA) application. CaWRKY70 overexpression promotes susceptibility in resistant chickpea (WR315) plants to Foc1 infection. Transgenic plants upon Foc1 inoculation demonstrated suppression of not only endogenous SA concentrations but expression of genes involved in SA signaling. CaWRKY70 overexpressing chickpea roots exhibited higher ion-leakage and Foc1 biomass accumulation compared to control transgenic (VC) plants. CaWRKY70 overexpression suppresses H2O2 production and resultant reactive oxygen species (ROS) induced cell death in Foc1 infected chickpea roots, stem and leaves. Being the nuclear targeted protein, CaWRKY70 suppresses CaMPK9-CaWRKY40 signaling in chickpea through its direct and indirect negative regulatory activities. Protein-protein interaction study revealed CaWRKY70 and CaRPP2-like CC-NB-ARC-LRR protein suppresses hyper-immune signaling in chickpea. Together, our study provides novel insights into mechanisms of suppression of the multiple defense signaling components in chickpea by CaWRKY70 under Foc1 stress. CaWRKY70 mediated defense suppression unveils networking between several immune signaling events negatively affecting downstream resistance mechanisms in chickpea under Foc1 stress.

中文翻译：

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CaWRKY70转录因子对多种防御反应途径的抑制作用提高了尖孢镰刀菌胁迫条件下鹰嘴豆的敏感性。

植物防御基因的抑制和激活受WRKY家族转录因子的全面调控。鹰嘴豆是一种非典型农作物豆类，因枯萎镰刀菌f引起枯萎。sp。ciceri Race1（Foc1），其防御反应机制了解甚少。在这里，我们试图显示WRKY70与参与Foc1攻击的鹰嘴豆易感性/抗性应答中涉及的几个下游信号传导组件之间的相互作用。在本研究中，我们发现Cicer arietinum L. WRKY70（CaWRKY70）对Foc1感染后鹰嘴豆中的多种防御反应途径（包括系统获得性抗性（SAR）激活）起负调控作用。在Foc1胁迫和水杨酸（SA）应用下，发现CaWRKY70在易感（JG62）鹰嘴豆的芽组织中大量积累。CaWRKY70过表达促进抗性鹰嘴豆（WR315）植物对Foc1感染的敏感性。Foc1接种后的转基因植物不仅抑制了内源性SA浓度，而且抑制了参与SA信号转导的基因的表达。与对照转基因（VC）植物相比，CaWRKY70过表达的鹰嘴豆根表现出更高的离子泄漏和Foc1生物量积累。CaWRKY70的过表达抑制Foc1感染的鹰嘴豆根，茎和叶中H2O2的产生和由此产生的活性氧（ROS）诱导的细胞死亡。作为核靶向蛋白，CaWRKY70通过其直接和间接的负调控作用抑制鹰嘴豆中的CaMPK9-CaWRKY40信号传导。蛋白质-蛋白质相互作用研究表明，CaWRKY70和CaRPP2-like CC-NB-ARC-LRR蛋白抑制鹰嘴豆中的超免疫信号。总之，我们的研究为FOC1胁迫下CaWRKY70抑制鹰嘴豆中多种防御信号成分的机制提供了新颖的见解。CaWRKY70介导的防御抑制揭示了在Foc1胁迫下对鹰嘴豆下游抗性机制产生负面影响的几个免疫信号事件之间的网络。