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Fis suppresses late-stage virulence gene expression in Yersinia pseudotuberculosis at environmental temperatures

ABSTRACT: The nucleoid-associated protein Fis is a key transcriptional regulator in Gram-negative bacteria that supports rapid adaptation to environmental changes. In Yersinia pseudotuberculosis, Fis plays a critical, yet poorly understood role in virulence. Here, we present a comparative transcriptomic analysis of Y. pseudotuberculosis wild type and fis deletion mutant at environmental (25°C) and host-relevant (37°C) temperatures. Our data show that Fis modulates the expression of more than 600 genes across 16 functional categories. Notably, Fis exerts reciprocal, temperature-dependent control over virulence genes, including those encoding the type III secretion system (T3SS) and Yersinia effector proteins (Yops), flagella biosynthesis, and cell adherence/invasion factors. Functional assays revealed that fis deletion disrupts this regulatory balance, producing a host-defense-like state at 25°C characterized by complete loss of motility, upregulation of the virulence master regulator LcrF, aberrant Yop secretion, impaired phagocytosis by host cells, and increased pathogenicity in the Galleria mellonella infection model. These findings establish Fis as a central regulator that coordinates motility and early host-cell engagement while preventing premature activation of antiphagocytic defenses, thereby optimizing the initial stages of infection.

ORGANISM(S): Yersinia pseudotuberculosis YPIII

PROVIDER: GSE295938 | GEO | 2026/03/16

REPOSITORIES: GEO

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Project description:Many species of pathogenic bacteria harbor critical plasmid-encoded virulence factors, and yet the regulation of plasmid replication is often poorly understood despite playing key role in plasmid-encoded gene expression. Human pathogenic Yersinia, including the plague agent Yersinia. pestis and its close relative Y. pseudotuberculosis, require the type III secretion system (T3SS) virulence factor to subvert host defense mechanisms and colonize host tissues. The Yersinia T3SS is encoded on the IncFII plasmid for Yersinia virulence (pYV). Several layers of gene regulation enables a large increase in expression of Yersinia T3SS genes at mammalian body temperature. Surprisingly, T3SS expression is also controlled at the level of gene dosage. The number of pYV molecules relative to the number of chromosomes per cell, referred to as plasmid copy number, increases with temperature. The ability to increase and maintain elevated pYV plasmid copy number, and therefore T3SS gene dosage, at 37˚C is important for Yersinia virulence. In addition, pYV is highly stable in Yersinia at all temperatures, despite being dispensable for growth outside the host. Yet how Yersinia reinforces elevated plasmid replication and plasmid stability remains unclear. In this study, we show that the chromosomal gene pcnB encoding the polyadenylase PAP I is required for regulation of pYV plasmid copy number (PCN), maintenance of pYV in the bacterial population outside the host, robust T3SS activity, and Yersinia virulence in a mouse infection model. Likewise, pcnB/PAP I is also required for robust expression of the Shigella flexneri virulence plasmid-encoded T3SS that, similar to Yersinia, is encoded on a virulence plasmid whose replication is regulated by sRNA. Furthermore, Yersinia and Shigella pcnB/PAP I is required for maintaining normal PCN of model antimicrobial resistance (AMR) plasmids whose replication is regulated by sRNA, thereby increasing antibiotic resistance by ten-fold. These data suggest that pcnB/PAP I contributes to the spread and stabilization of sRNA-regulated virulence and AMR plasmids in bacterial pathogens, and is essential in maintaining the gene dosage required to mediate plasmid-encoded traits. Importantly pcnB/PAP I has been bioinformatically identified in many species of bacteria despite being studied in only a few species to date. Our work highlights the potential importance of pcnB/PAP I in antibiotic resistance, and shows for the first time that pcnB/PAP I reinforces PCN andpromotes virulence plasmid stability in natural pathogenic hosts with a direct impact on bacterial virulence.

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Fis suppresses late-stage virulence gene expression in Yersinia pseudotuberculosis at environmental temperatures

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