Du Meixia, Wang Shuai, Dong Liting, Qu Rongrong, Zheng Lin, He Yongrui, Chen Shanchun, Zou Xiuping
National Citrus Engineering Research Center, Citrus Research Institute, Southwest University, Chongqing, China.
Front Microbiol. 2022 Feb 21;12:797841. doi: 10.3389/fmicb.2021.797841. eCollection 2021.
Huanglongbing (HLB), caused by " liberibacter asiaticus" (Las), is one of the most devastating diseases in citrus but its pathogenesis remains poorly understood. Here, we reported the role of the LasSDE115 (CLIBASIA_05115) effector, encoded by Las, during pathogen-host interactions. Bioinformatics analyses showed that LasSDE115 was 100% conserved in all reported Las strains but had sequence differences compared with orthologs from other " liberibacter." Prediction of protein structures suggested that the crystal structure of LasSDE115 was very close to that of the invasion-related protein B (IalB), a virulence factor from . Alkaline phosphatase (PhoA) assay in further confirmed that LasSDE115 was a Sec-dependent secretory protein while subcellular localization analyses in tobacco showed that the mature protein of SDE115 (mSDE115), without its putative Sec-dependent signal peptide, was distributed in the cytoplasm and the nucleus. Expression levels of in Las-infected Asian citrus psyllid (ACP) were much higher (∼45-fold) than those in Las-infected Wanjincheng oranges, with the expression in symptomatic leaves being significantly higher than that in asymptomatic ones. Additionally, the overexpression of favored Las proliferation during the early stages (2 months) of infection while promoting the development of symptoms. Hormone content and gene expression analysis of transgenic plants also suggested that overexpressing modulated the transcriptional regulation of genes involved in systemic acquired resistance (SAR) response. Overall, our data indicated that LasSDE115 effector contributed to the early colonization of citrus by the pathogen and worsened the occurrence of Huanglongbing symptoms, thereby providing a theoretical basis for further exploring the pathogenic mechanisms of Huanglongbing disease in citrus.
柑橘黄龙病(HLB)由“亚洲韧皮杆菌”(Las)引起,是柑橘中最具毁灭性的病害之一,但其发病机制仍知之甚少。在此,我们报道了Las编码的效应蛋白LasSDE115(CLIBASIA_05115)在病原体与宿主相互作用中的作用。生物信息学分析表明,LasSDE115在所有已报道的Las菌株中100%保守,但与其他“韧皮杆菌”的直系同源物存在序列差异。蛋白质结构预测表明,LasSDE115的晶体结构与入侵相关蛋白B(IalB)非常接近,IalB是一种来自[此处原文缺失相关信息]的毒力因子。[此处原文缺失相关实验主体]中的碱性磷酸酶(PhoA)检测进一步证实LasSDE115是一种依赖Sec的分泌蛋白,而烟草中的亚细胞定位分析表明,去除假定的依赖Sec信号肽后的SDE115成熟蛋白(mSDE115)分布在细胞质和细胞核中。Las感染的亚洲柑橘木虱(ACP)中[此处原文缺失相关基因名称]的表达水平比Las感染的温州蜜柑高得多(约45倍),有症状叶片中的表达明显高于无症状叶片。此外,[此处原文缺失相关基因名称]的过表达在感染早期(2个月)有利于Las增殖,同时促进症状发展。转基因植物的激素含量和基因表达分析还表明,过表达[此处原文缺失相关基因名称]可调节参与系统获得性抗性(SAR)反应的基因转录调控。总体而言,我们的数据表明LasSDE115效应蛋白有助于病原体在柑橘中的早期定殖,并加剧柑橘黄龙病症状的发生,从而为进一步探索柑橘黄龙病的致病机制提供了理论依据。