Brucella melitensis VjbR and C12-HSL regulons: contributions of the N-dodecanoyl homoserine lactone signaling molecule and LuxR homologue VjbR to gene expression.
Brucella melitensis VjbR and C12-HSL regulons: contributions of the N-dodecanoyl homoserine lactone signaling molecule and LuxR homologue VjbR to gene expression.
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DOI：
10.1186/1471-2180-10-167
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发表时间：
2010-06-08
期刊：
影响因子：
4.2
通讯作者：
Ficht TA
中科院分区：
文献类型：
--
作者：
Weeks JN;Galindo CL;Drake KL;Adams GL;Garner HR;Ficht TA
群体感应是一种通讯系统，它调节基因的表达以响应种群密度，并经常调节毒力决定因素。LUXR同源基因vjbR的缺失会显著降低羊种布鲁氏菌的细胞内存活，并被解释为QS在布鲁氏菌感染中的作用。布鲁氏菌培养的体外合成自身诱导物(AI)的实验表明，这种作用得到了证实，但没有得到证实。为了进一步阐明VjbR在毒力和生存中的作用，利用基因芯片分析了VjbR和AI调控下的基因表达。对野生型和等基因ΔvjbR转移体在外源N-十二酰高丝氨酸内酯(C12-HSL)存在和不存在的情况下生长的分析揭示了基因调控的时间模式，在指数生长期和平稳生长期检测到差异。VjbR和C12-HSL转录本的比较表明，除3个基因外，其余127个基因共同调控，表明C12-HSL通过VjbR逆转这些基因的表达。对ΔvjbR突变体的进一步分析表明，在没有vjbR的情况下，ahl也改变了基因的表达，在生长稳定期上调了48个基因和一个LuxR同源物blxR的表达93倍。基因表达变化包括以前未被描述的粘附素、蛋白酶、抗生素和毒素抗性基因、逆境生存辅助基因、转运蛋白、膜生物发生基因、氨基酸代谢和运输、转录调节基因、能量产生基因以及先前报道的FliF和VIRB操纵子。VjbR和C12-HSL调节大量不同数量的基因的表达。许多在其他细菌病原体中被鉴定为毒力因子的基因被发现有不同的表达，这表明布鲁氏菌在细胞内的存活有重要的贡献。根据这些数据，我们得出结论，VjbR和C12-HSL通过调节毒力机制的表达，从而控制细菌在宿主细胞内的生存能力，从而促进毒力和生存。一种可能的情况是通过QS发生的，然而，这种机制的操作仍有待演示。
Quorum sensing is a communication system that regulates gene expression in response to population density and often regulates virulence determinants. Deletion of the luxR homologue vjbR highly attenuates intracellular survival of Brucella melitensis and has been interpreted to be an indication of a role for QS in Brucella infection. Confirmation for such a role was suggested, but not confirmed, by the demonstrated in vitro synthesis of an auto-inducer (AI) by Brucella cultures. In an effort to further delineate the role of VjbR to virulence and survival, gene expression under the control of VjbR and AI was characterized using microarray analysis. Analyses of wildtype B. melitensis and isogenic ΔvjbR transciptomes, grown in the presence and absence of exogenous N-dodecanoyl homoserine lactone (C12-HSL), revealed a temporal pattern of gene regulation with variances detected at exponential and stationary growth phases. Comparison of VjbR and C12-HSL transcriptomes indicated the shared regulation of 127 genes with all but 3 genes inversely regulated, suggesting that C12-HSL functions via VjbR in this case to reverse gene expression at these loci. Additional analysis using a ΔvjbR mutant revealed that AHL also altered gene expression in the absence of VjbR, up-regulating expression of 48 genes and a luxR homologue blxR 93-fold at stationary growth phase. Gene expression alterations include previously un-described adhesins, proteases, antibiotic and toxin resistance genes, stress survival aids, transporters, membrane biogenesis genes, amino acid metabolism and transport, transcriptional regulators, energy production genes, and the previously reported fliF and virB operons. VjbR and C12-HSL regulate expression of a large and diverse number of genes. Many genes identified as virulence factors in other bacterial pathogens were found to be differently expressed, suggesting an important contribution to intracellular survival of Brucella. From these data, we conclude that VjbR and C12-HSL contribute to virulence and survival by regulating expression of virulence mechanisms and thus controlling the ability of the bacteria to survive within the host cell. A likely scenario occurs via QS, however, operation of such a mechanism remains to be demonstrated.
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影响因子：
3.1
作者：
Allen, CA;Adams, LG;Ficht, TA
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