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首页> 外文期刊>Infection and immunity >Transcriptome Reprogramming by Plasmid-Encoded Transcriptional Regulators Is Required for Host Niche Adaption of a Macrophage Pathogen
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Transcriptome Reprogramming by Plasmid-Encoded Transcriptional Regulators Is Required for Host Niche Adaption of a Macrophage Pathogen

机译：质粒编码的转录调节子的转录组重编程是巨噬细胞病原体宿主生态位适应所必需的。

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Rhodococcus equi is a facultative intracellular pathogen of macrophages, relying on the presence of a conjugative virulence plasmid harboring a 21-kb pathogenicity island (PAI) for growth in host macrophages. The PAI encodes a family of 6 virulence-associated proteins (Vaps) in addition to 20 other proteins. The contribution of these to virulence has remained unclear. We show that the presence of only 3 virulence plasmid genes (of 73 in total) is required and sufficient for intracellular growth. These include a single vap family member, vapA, and two PAI-located transcriptional regulators, virR and virS. Both transcriptional regulators are essential for wild-type-level expression of vapA, yet vapA expression alone is not sufficient to allow intracellular growth. A whole-genome microarray analysis revealed that VirR and VirS substantially integrate themselves into the chromosomal regulatory network, significantly altering the transcription of 18% of all chromosomal genes. This pathoadaptation involved significant enrichment of select gene ontologies, in particular, enrichment of genes involved in transport processes, energy production, and cellular metabolism, suggesting a major change in cell physiology allowing the bacterium to grow in the hostile environment of the host cell. The results suggest that following the acquisition of the virulence plasmid by an avirulent ancestor of R. equi, coevolution between the plasmid and the chromosome took place, allowing VirR and VirS to regulate the transcription of chromosomal genes in a process that ultimately promoted intracellular growth. Our findings suggest a mechanism for cooption of existing chromosomal traits during the evolution of a pathogenic bacterium from an avirulent saprophyte.
机译：马红球菌是巨噬细胞的兼性细胞内病原体，依赖于带有21kb致病性岛（PAI）的结合毒力质粒的存在，以在宿主巨噬细胞中生长。除20种其他蛋白外，PAI还编码6种与毒力相关的蛋白（Vaps）家族。这些对毒力的贡献仍不清楚。我们显示，仅存在3个毒力质粒基因（总共73个），对于细胞内生长而言是足够的。其中包括一个单一的 vap 家族成员 vapA ，以及两个位于PAI上的转录调节子 virR 和 virS 。两种转录调节子对于 vapA 的野生型表达都是必不可少的，但是仅 vapA 的表达不足以允许细胞内生长。全基因组微阵列分析显示，VirR和VirS基本上将自身整合到染色体调节网络中，从而显着改变了所有染色体基因中18％的转录。这种病理适应涉及选择基因本体的显着富集，特别是涉及运输过程，能量产生和细胞代谢的基因的富集，表明细胞生理学的重大变化，使细菌能够在宿主细胞的不利环境中生长。结果表明，在由无毒的马齿。的无性祖先获得毒性质粒后，质粒与染色体之间发生了共同进化，从而使VirR和VirS在最终促进细胞内生长的过程中调节了染色体基因的转录。我们的发现提出了在无毒腐生植物致病细菌进化过程中现有染色体性状的共存机制。

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