很多革兰氏阴性病原细菌的致病性依赖于III型分泌系统（T3SS）。植物病原细菌的T3SS由hrp基因簇编码。非编码RNA是近十多年来发现的一类影响很多细胞过程的重要调控因子。在人及动物病原细菌中已鉴定到50多个与致病相关的非编码RNA，但至今只报道了5个与植物病原细菌致病相关的非编码RNA，而且其中的4个的作用机理还不清楚。十字花科黑腐病菌（Xcc）是研究植物病原菌致病分子机理的重要模式菌之一。本课题组在完成了Xcc全基因组非编码RNA的鉴定后，发现非编码RNA SR220调控hrp基因的表达。过量表达SR220会显著增加Xcc所有hrp基因mRNA的量。SR220是一新的非编码RNA。本项目拟通过RNA互作组俘获、转录组和蛋白组分析等，鉴定SR220的直接靶标，解析它们的互作方式及调控hrp基因表达的分子机理。研究结果对全面认识植物病原细菌致病性的调控机理具有重要意义。

The pathogenicity of many Gram-negative bacterial pathogens relies on the type III secretion system (T3SS). The T3SS in phytopathogenic bacteria is encoded by the conserved hrp (hypersensitive response and pathogenicity) gene cluster which consists of more than twenty genes in five to six main operons. In the recent decade, it has been demonstrated that non-coding RNAs act as important factors regulating various cellular processes. To date, more than fifty virulence-related non-coding RNAs have been identified from human and animal bacterial pathogens; however, little is known about their role in the pathogenicity of plant bacterial pathogens. So far, only five virulence-related non-coding RNAs have been reported and of which the regulatory mechanism of four in pathogenesis is uncovered yet. We have studied the regulation mechanism of hrp gene expression using Xanthomonas campestris pv. campestris (Xcc) as a model for many years. Recently, after genome-wide identification of the non-coding RNAs from Xcc, we found that the non-coding RNA SR220 is involved in the regulation of hrp gene expression. Over-expression of SR220 in Xcc resulted in a significant increase in mRNA production of all hrp genes. Bioinformatics analysis revealed that SR220 is a novel non-coding RNA. The aims of this work are: (1) to identify the direct binding targets of SR220 by RNA interactome capture, transcriptome and proteome analyses; (2) to study the manner by which SR220 interacts with its targets; (3) finally, to clarify the molecular mechanism by which SR220 regulates hrp gene expression. The result will facilitate our understanding of the regulatory mechanism of pathogenicity in plant bacterial pathogens.