XerR调控xccR/pip遗传位点表达工作模型
群体感应(Quorum sensing，QS)是细菌根据自身分泌的信号分子的浓度感应细胞密度进而产生细菌群体行为的基因调控方式。由信号分子介导的信号传递途径不仅发生在细菌之间，也存在于真核生物与细菌之间。
野油菜黄单胞菌（Xanthomonas campestris pv. campestris, Xcc）是导致多种十字花科植物发生黑腐病的一种模式致病菌。中科院微生物研究所方荣祥院士课题组的研究表明，xccR/pip是Xcc致病相关的遗传位点。在寄主植物甘蓝中，Xcc的致病因子PIP（脯氨酸亚氨基肽酶）基因表达受到上游群体感应调节因子XccR诱导。
方荣祥院士课题组贾燕涛博士通过最新研究，发现一个XccR表达的抑制子XerR，XerR蛋白能够直接和xccR启动子探针结合抑制XccR表达。有趣的是，在植物体内，超表达XerR菌株其xccR的表达不但没有降低，xccR和pip的转录水平反而更接近野生型，说明XerR对XccR的抑制作用被解除。
课题组人员试图了解超表达XerR的菌株是如何解除对xccR基因表达的抑制作用，又进一步开展了体外结合实验。实验结果证明：XerR对xccR/pip表达的去抑制是由于植物信号的参与引起的。植物中某种分子量小于1KD的水提取物解离了XerR蛋白和DNA的相互作用，同时，该水提取物还促进了XccR与pip启动子DNA序列的结合效率。
这是第一次有文献报道植物病原菌对植物产生的信号分子产生感应，从而成功侵染宿主。科研人员推测，细菌在长期进化过程中，形成了一类通过跨界感应植物信号分子的独特的群体感应信号转导机制，适应了植物的生存环境，并最终达到细菌致病的目的。
该项目得到了国家自然科学基金项目和科技部973项目的支持。相关论文4月12日在线发表在《细胞研究》（Cell Research）上。（生物谷Bioon.com）
生物谷推荐原文出处：
Cell Research , (12 April 2011) | doi:10.1038/cr.2011.64
XerR, a negative regulator of XccR in Xanthomonas campestris pv. campestris, relieves its repressor function in planta
Li Wang, Lili Zhang, Yunfeng Geng, Wei Xi, Rongxiang Fang and Yantao Jia
AbstractWe previously reported that XccR, a LuxR-type regulator of Xanthomonas campestris pv. campestris (Xcc), activates the downstream proline iminopeptidase virulence gene (pip) in response to certain host plant factor(s). In this report, we further show that the expression of the xccR gene was repressed in the culture medium by an NtrC-type response regulator, which we named XerR (XccR expression-related, repressor), and that this repression was relieved when the bacteria were grown in planta. Such a regulatory mechanism is reinforced by the observations that XerR directly bound to the xccR promoter in vitro, and that mutations at the phosphorylation-related residues of XerR resulted in the loss of its repressor function. Furthermore, the expression level of xccR increased even in XerR-overexpressing Xcc cells when they were vacuum infiltrated into cabbage plants. We also preliminarily characterized the host factor(s) involved in the above mentioned interactions between Xcc and the host plant, showing that a plant material(s) with molecular weight(s) less than 1 kDa abolished the binding of XerR to the xccR promoter, while the same material enhanced the binding of XccR to the luxXc box in the pip promoter. Taken together, our results implicate XerR in a new layer of the regulatory mechanism controlling the expression of the virulence-related xccR/pip locus and provide clues to the identification of plant signal molecules that interact with XerR and XccR to enhance the virulence of Xcc.
