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基因表达与酰高丝氨酸内酯信号在 中的关系。

The relationship between gene expression and acylhomoserine lactone signaling in .

机构信息

Department of Microbiology, University of Washington School of Medicine, Seattle, Washington, USA.

出版信息

J Bacteriol. 2024 Oct 24;206(10):e0013824. doi: 10.1128/jb.00138-24. Epub 2024 Sep 5.

Abstract

The opportunistic pathogen has complex quorum sensing (QS) circuitry, which involves two acylhomoserine lactone (AHL) systems, the LasI AHL synthase and LasR AHL-dependent transcriptional activator system and the RhlI AHL synthase-RhlR AHL-responsive transcriptional activator. There is also a quinoline signaling system [the quinolone signal (PQS) system]. Although there is a core set of genes regulated by the AHL circuits, there is strain-to-strain variation in the non-core QS regulon. A size reduction of the QS regulon occurs in laboratory evolution experiments with the model strain PAO1. We used transcriptomics to test the hypothesis that reductive evolution in the PAO1 QS regulon can in large part be explained by a null mutation in , the gene encoding the transcriptional activator of the operon. We found that PqsR had very little influence on the AHL QS regulon. This was a surprising finding because the last gene in the PqsR-dependent operon, , codes for a protein, which physically interacts with RhlR, and this interaction is required for RhlR-dependent activation of some genes. We used comparative transcriptomics to examine the influence of a mutation on the QS regulon and identified only three transcripts, which were strictly dependent on PqsE. By using reporter constructs, we showed that the PqsE influence on other genes was dependent on experimental conditions and we have gained some insight about those conditions. This work adds to our understanding of the plasticity of the QS regulon and to the role PqsE plays in RhlR-dependent gene activation.IMPORTANCEOver many generations of growth in certain conditions, undergoes a large reductive evolution in the number of genes activated by quorum sensing. Here, we rule out one plausible route of the reductive evolution: that a mutation in a transcriptional activator PqsR or the PqsR activation of , which codes for a chaperone for the quorum sensing signal-responsive transcription factor RhlR, explains the finding. We further provide information about the influence of PqsR and PqsE on quorum sensing in .

摘要

机会性病原体具有复杂的群体感应(QS)电路,其中涉及两个酰基高丝氨酸内酯(AHL)系统,LasI AHL 合酶和 LasR AHL 依赖性转录激活系统,以及 RhlI AHL 合酶-RhlR AHL 响应转录激活系统。还有一个喹啉信号系统[喹啉信号(PQS)系统]。尽管有一组核心基因受 AHL 电路调节,但非核心 QS 调节子在菌株间存在差异。在模型菌株 PAO1 的实验室进化实验中,QS 调节子的大小会缩小。我们使用转录组学来检验以下假设:PAO1 QS 调节子的简化进化在很大程度上可以用编码 基因的缺失突变来解释,该基因是 操纵子的转录激活因子。我们发现 PqsR 对 AHL QS 调节子的影响很小。这是一个令人惊讶的发现,因为 PqsR 依赖性 操纵子中的最后一个基因 编码一种蛋白质,该蛋白质与 RhlR 物理相互作用,这种相互作用是 RhlR 依赖激活某些基因所必需的。我们使用比较转录组学来研究 突变对 QS 调节子的影响,仅鉴定出三个严格依赖于 PqsE 的转录本。通过使用报告基因构建体,我们表明 PqsE 对其他基因的影响取决于实验条件,并且我们已经对这些条件有了一些了解。这项工作增加了我们对 QS 调节子的可塑性以及 PqsE 在 RhlR 依赖基因激活中的作用的理解。

重要性:
在某些条件下经过多代生长后, 通过群体感应激活的基因数量发生了大规模的简化进化。在这里,我们排除了简化进化的一种可能途径:转录激活因子 PqsR 的突变或 PqsR 对 的激活,后者编码群体感应信号响应转录因子 RhlR 的伴侣,这解释了这一发现。我们进一步提供了有关 PqsR 和 PqsE 在 中对群体感应影响的信息。

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