Shanghai Yangtze River Delta Eco-Environmental Change and Management Observation and Research Station, Ministry of Science and Technology, Ministry of Education, Shanghai Urban Forest Ecosystem Research Station, National Forestry and Grassland Administration, Shanghai Cooperative Innovation Center for Modern Seed Industry, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, China.
Department of Environmental Sciences, COMSATS University Islamabad, Vehari Campus, Vehari, Pakistan.
PLoS Pathog. 2021 Jul 23;17(7):e1009762. doi: 10.1371/journal.ppat.1009762. eCollection 2021 Jul.
Pathogens integrate multiple environmental signals to navigate the host and control the expression of virulence genes. In this process, small regulatory noncoding RNAs (sRNAs) may function in gene expression as post-transcriptional regulators. In this study, the sRNA Xonc3711 functioned in the response of the rice pathogen, Xanthomonas oryzae pv. oryzicola (Xoc), to oxidative stress. Xonc3711 repressed production of the DNA-binding protein Xoc_3982 by binding to the xoc_3982 mRNA within the coding region. Mutational analysis showed that regulation required an antisense interaction between Xonc3711 and xoc_3982 mRNA, and RNase E was needed for degradation of the xoc_3982 transcript. Deletion of Xonc3711 resulted in a lower tolerance to oxidative stress due to the repression of flagella-associated genes and reduced biofilm formation. Furthermore, ChIP-seq and electrophoretic mobility shift assays showed that Xoc_3982 repressed the transcription of effector xopC2, which contributes to virulence in Xoc BLS256. This study describes how sRNA Xonc3711 modulates multiple traits in Xoc via signals perceived from the external environment.
病原体整合多种环境信号来在宿主中导航并控制毒力基因的表达。在这个过程中，小调控非编码 RNA（sRNA）可能作为转录后调控因子在基因表达中发挥作用。在这项研究中，水稻病原菌稻黄单胞菌 pv. 稻生致病变种（Xoc）中的 sRNA Xonc3711 参与了氧化应激反应。Xonc3711 通过结合编码区内的 xoc_3982 mRNA 来抑制 DNA 结合蛋白 Xoc_3982 的产生。突变分析表明，调控需要 Xonc3711 和 xoc_3982 mRNA 之间的反义相互作用，并且需要 RNase E 来降解 xoc_3982 转录本。由于鞭毛相关基因的抑制和生物膜形成减少，Xonc3711 的缺失导致对氧化应激的耐受性降低。此外，ChIP-seq 和电泳迁移率变动分析表明，Xoc_3982 抑制了效应因子 xopC2 的转录，而 xopC2 对 Xoc BLS256 的毒力有贡献。本研究描述了 sRNA Xonc3711 如何通过从外部环境感知的信号来调节 Xoc 中的多种性状。
