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两种增强子结合蛋白激活细菌共生体中一个群体调节 RNA 的 σ 依赖性转录。

Two enhancer binding proteins activate σ-dependent transcription of a quorum regulatory RNA in a bacterial symbiont.

机构信息

Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, United States.

Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, United States.

出版信息

Elife. 2023 May 5;12:e78544. doi: 10.7554/eLife.78544.

DOI:10.7554/eLife.78544
PMID:37145113
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10162802/
Abstract

To colonize a host, bacteria depend on an ensemble of signaling systems to convert information about the various environments encountered within the host into specific cellular activities. How these signaling systems coordinate transitions between cellular states in vivo remains poorly understood. To address this knowledge gap, we investigated how the bacterial symbiont initially colonizes the light organ of the Hawaiian bobtail squid . Previous work has shown that the small RNA Qrr1, which is a regulatory component of the quorum-sensing system in , promotes host colonization. Here, we report that transcriptional activation of Qrr1 is inhibited by the sensor kinase BinK, which suppresses cellular aggregation by prior to light organ entry. We show that Qrr1 expression depends on the alternative sigma factor σ and the transcription factors LuxO and SypG, which function similar to an OR logic gate, thereby ensuring Qrr1 is expressed during colonization. Finally, we provide evidence that this regulatory mechanism is widespread throughout the family. Together, our work reveals how coordination between the signaling pathways underlying aggregation and quorum-sensing promotes host colonization, which provides insight into how integration among signaling systems facilitates complex processes in bacteria.

摘要

为了在宿主中定植,细菌依赖于一系列信号系统,将其在宿主中遇到的各种环境信息转化为特定的细胞活动。这些信号系统如何协调体内细胞状态的转变在很大程度上仍不清楚。为了解决这一知识空白,我们研究了细菌共生体 最初如何定植夏威夷短尾乌贼的发光器官 。先前的研究表明,小 RNA Qrr1 是 群体感应系统的调控成分,可促进宿主定植。在这里,我们报告说,BinK 传感器激酶抑制 Qrr1 的转录激活,BinK 在进入发光器官之前抑制细胞聚集。我们表明 Qrr1 的表达依赖于替代 sigma 因子 σ 和转录因子 LuxO 和 SypG,它们的作用类似于或门逻辑门,从而确保 Qrr1 在定植期间表达。最后,我们提供了证据表明,这种调控机制在整个 家族中广泛存在。总之,我们的工作揭示了聚集和群体感应信号通路之间的协调如何促进宿主定植,这为整合信号系统如何促进细菌的复杂过程提供了深入了解。

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