State Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crops, College of Plant Protection, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Institute of Oceanography, Minjiang University, Fuzhou 350108, China.
Int J Mol Sci. 2020 Oct 27;21(21):7996. doi: 10.3390/ijms21217996.
' Liberibacter asiaticus' (CLas) is the pathogenic bacterium that causes the disease Huanglongbing (HLB) in citrus and some model plants, such as . After infection, CLas releases a set of effectors to modulate host responses. One of these critical effectors is Sec-delivered effector 1 (SDE1), which induces chlorosis and cell death in . In this study, we revealed the DEAD-box RNA helicase (DDX3) interacts with SDE1. Gene silencing study revealed that knockdown of the gene triggers leaf chlorosis, mimicking the primary symptom of CLas infection in . The interactions between SDE1 and NbDDX3 were localized in the cell membrane. Overexpression of resulted in suppression of gene expression in , which suggests a critical role of in modulating expression. Furthermore, we verified the interaction of SDE1 with citrus DDX3 (CsDDX3), and demonstrated that the expression of the gene was significantly reduced in HLB-affected yellowing and mottled leaves of citrus. Thus, we provide molecular evidence that the downregulation of the host gene is a crucial mechanism of leaf chlorosis in HLB-affected plants. The identification of CsDDX3 as a critical target of SDE1 and its association with HLB symptom development indicates that the gene is an important target for gene editing, to interrupt the interaction between DDX3 and SDE1, and therefore interfere host susceptibility.
'亚洲韧皮杆菌'(CLas)是引起柑橘黄龙病(HLB)和一些模式植物病害的致病细菌,如. 感染后,CLas 释放一组效应物来调节宿主反应。其中一种关键效应物是Sec 输送效应物 1(SDE1),它在. 中诱导黄化和细胞死亡。在本研究中,我们揭示了 DEAD 盒 RNA 解旋酶(DDX3)与 SDE1 相互作用。基因沉默研究表明, 基因的敲低会引发叶片黄化,模拟 CLas 感染. 中的主要症状。SDE1 和 NbDDX3 之间的相互作用定位于细胞膜上。过表达 导致. 中 基因表达受到抑制,这表明 在调节 表达中起关键作用。此外,我们验证了 SDE1 与柑橘 DDX3(CsDDX3)的相互作用,并证明在柑橘 HLB 发病的黄化和斑驳叶片中, 基因的表达显著降低。因此,我们提供了分子证据,表明宿主 基因的下调是 HLB 感染植物叶片黄化的一个关键机制。鉴定 CsDDX3 为 SDE1 的关键靶标及其与 HLB 症状发展的关联表明, 基因是基因编辑的一个重要靶标,可中断 DDX3 和 SDE1 之间的相互作用,从而干扰宿主易感性。