XerR調(diào)控xccR/pip遺傳位點表達工作模型

群體感應(yīng)(Quorum sensing，QS)是細菌根據(jù)自身分泌的信號分子的濃度感應(yīng)細胞密度進而產(chǎn)生細菌群體行為的基因調(diào)控方式,。由信號分子介導(dǎo)的信號傳遞途徑不僅發(fā)生在細菌之間,，也存在于真核生物與細菌之間。

野油菜黃單胞菌（Xanthomonas campestris pv. campestris, Xcc）是導(dǎo)致多種十字花科植物發(fā)生黑腐病的一種模式致病菌,。中科院微生物研究所方榮祥院士課題組的研究表明,，xccR/pip是Xcc致病相關(guān)的遺傳位點。在寄主植物甘藍中,，Xcc的致病因子PIP（脯氨酸亞氨基肽酶）基因表達受到上游群體感應(yīng)調(diào)節(jié)因子XccR誘導(dǎo),。

方榮祥院士課題組賈燕濤博士通過最新研究，發(fā)現(xiàn)一個XccR表達的抑制子XerR,，XerR蛋白能夠直接和xccR啟動子探針結(jié)合抑制XccR表達,。有趣的是，在植物體內(nèi),，超表達XerR菌株其xccR的表達不但沒有降低,，xccR和pip的轉(zhuǎn)錄水平反而更接近野生型，說明XerR對XccR的抑制作用被解除,。

課題組人員試圖了解超表達XerR的菌株是如何解除對xccR基因表達的抑制作用,，又進一步開展了體外結(jié)合實驗。實驗結(jié)果證明：XerR對xccR/pip表達的去抑制是由于植物信號的參與引起的,。植物中某種分子量小于1KD的水提取物解離了XerR蛋白和DNA的相互作用,，同時，該水提取物還促進了XccR與pip啟動子DNA序列的結(jié)合效率,。

這是第一次有文獻報道植物病原菌對植物產(chǎn)生的信號分子產(chǎn)生感應(yīng),，從而成功侵染宿主?？蒲腥藛T推測,，細菌在長期進化過程中，形成了一類通過跨界感應(yīng)植物信號分子的獨特的群體感應(yīng)信號轉(zhuǎn)導(dǎo)機制,，適應(yīng)了植物的生存環(huán)境,，并最終達到細菌致病的目的。

該項目得到了國家自然科學(xué)基金項目和科技部973項目的支持,。相關(guān)論文4月12日在線發(fā)表在《細胞研究》（Cell Research）上,。（生物谷Bioon.com）

生物谷推薦原文出處：

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.