Yersinia pestis autoagglutination factor is a component of the type six secretion system

Podladchikova, O.; Antonenka, Uladz; Heesemann, Jürgen; Rakin, Alexander

doi:10.1016/j.ijmm.2011.03.004

Cited by 11 publications

(9 citation statements)

References 50 publications

(62 reference statements)

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“…However, it had no effect on virulence in bubonic or pneumonic murine plague models compared to the parental Y. pestis CO92 strain (Robinson et al, 2009 ; Andersson et al, 2017 ). An Hcp-like protein encoded by ypo0502 was found to play important roles in autoagglutination (AA), indicating that the T6SS Cluster A is involved in intraspecies interaction of bacteria (Podladchikova et al, 2011 ). A similar thermoregulated gene cluster in Y. pseudotuberculosis was identified as T6SS4 ( ypk_3548 - ypk_3566 ), which is precisely regulated by temperature, growth phase, and AHL-dependent quorum sensing systems, and plays a crucial role in resistance to environmental stresses (Zhang et al, 2011b ).…”

Section: Comparison Of T6ss Gene Clusters In Yersinia mentioning

confidence: 99%

Type VI Secretion Systems Present New Insights on Pathogenic Yersinia

Yang

Pan

Wang

et al. 2018

Front. Cell. Infect. Microbiol.

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The type VI secretion system (T6SS) is a versatile secretion system widely distributed in Gram-negative bacteria that delivers multiple effector proteins into either prokaryotic or eukaryotic cells, or into the extracellular milieu. T6SS participates in various physiological processes including bacterial competition, host infection, and stress response. Three pathogenic Yersinia species, namely Yersinia pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica, possess different copies of T6SSs with distinct biological functions. This review summarizes the pathogenic, antibacterial, and stress-resistant roles of T6SS in Yersinia and the ion-transporting ability in Y. pseudotuberculosis. In addition, the T6SS-related effectors and regulators identified in Yersinia are discussed.

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Section: Comparison Of T6ss Gene Clusters In Yersinia mentioning

confidence: 99%

Type VI Secretion Systems Present New Insights on Pathogenic Yersinia

Yang

Pan

Wang

et al. 2018

Front. Cell. Infect. Microbiol.

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“…The identification of T6SS in human pathogens can be traced back to seminal discoveries made in both Pseudomonas aeruginosa and Vibrio cholerae in which a cluster of chromosomally encoded genes have been found to be involved in bacterial virulence (Mougous et al, 2006;Pukatzki et al, 2006). Indeed, multiple copies of hcps and vgrGs have commonly been seen across all the bacteria that possess the T6SS, and, interestingly, some bacteria even possess multiple copies of the T6SS cluster (Mougous et al, 2006;Podladchikova et al, 2011). In A. hydrophila, the two effector proteins (Hcps and VgrGs) that disarm host defences by targeting genes important for innate immune cells (among other genes) cluster to only one region of the chromosome (Seshadri et al, 2006;Suarez et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the roles played by Hcp and VgrG type 6 secretion system effectors in Aeromonas hydrophila SSU pathogenesis

et al. 2013

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Aeromonas hydrophila, a Gram-negative bacterium, is an emerging human pathogen equipped with both a type 3 and a type 6 secretion system (T6SS). In this study, we evaluated the roles played by paralogous T6SS effector proteins, hemolysin co-regulated proteins (Hcp-1 and -2) and valine glycine repeat G (VgrG-1, -2 and -3) protein family members in A. hydrophila SSU pathogenesis by generating various combinations of deletion mutants of the their genes. In addition to their predicted roles as structural components and effector proteins of the T6SS, our data clearly demonstrated that paralogues of Hcp and VgrG also influenced bacterial motility, protease production and biofilm formation. Surprisingly, there was limited to no observed functional redundancy among and/or between the aforementioned T6SS effector paralogues in multiple assays. Our data indicated that Hcp and VgrG paralogues located within the T6SS cluster were more involved in forming T6SS structures, while the primary roles of Hcp-1 and VgrG-1, located outside of the T6SS cluster, were as T6SS effectors. In terms of influence on bacterial physiology, Hcp-1, but not Hcp-2, influenced bacterial motility and protease production, and in its absence, increases in both of the aforementioned activities were observed. Likewise, VgrG-1 played a major role in regulating bacterial protease production, while VgrG-2 and VgrG-3 were critical in regulating bacterial motility and biofilm formation. In an intraperitoneal murine model of infection, all Hcp and VgrG paralogues were required for optimal bacterial virulence and dissemination to mouse peripheral organs. Importantly, the observed phenotypic alterations of the T6SS mutants could be fully complemented. Taking these results together, we have further established the roles played by the two known T6SS effectors of A. hydrophila by defining their contributions to T6SS function and virulence in both in vitro and in vivo models of infection.

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“…The Y. pseudotuberculosis T6SS-4 has been reported to be upregulated by quorum sensing systems and in response to nutrient limitation and acidic, osmotic, and oxidative stress and to function in the transport of zinc ions (74), factors that may be relevant to biofilm growth. Of note, the Hcp protein of the Y. pestis T6SS-4 was reported to be an autoaggregation factor (75,76). However, we found that deletion of this hcp gene or of the entire T6SS-4 locus of Y. pestis did not significantly affect its autoaggregative phenotype (Fig.…”

Section: Differential Expression Of a Type VI Secretion System (T6ss)mentioning

confidence: 64%

Differential Gene Expression Patterns of Yersinia pestis and Yersinia pseudotuberculosis during Infection and Biofilm Formation in the Flea Digestive Tract

et al. 2019

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Yersinia pestis, the etiologic agent of plague, emerged as a fleaborne pathogen only within the last 6,000 years. Just five simple genetic changes in the Yersinia pseudotuberculosis progenitor, which served to eliminate toxicity to fleas and to enhance survival and biofilm formation in the flea digestive tract, were key to the transition to the arthropodborne transmission route. To gain a deeper understanding of the genetic basis for the development of a transmissible biofilm infection in the flea foregut, we evaluated additional gene differences and performed in vivo transcriptional profiling of Y. pestis, a Y. pseudotuberculosis wild-type strain (unable to form biofilm in the flea foregut), and a Y. pseudotuberculosis mutant strain (able to produce foregut-blocking biofilm in fleas) recovered from fleas 1 day and 14 days after an infectious blood meal. Surprisingly, the Y. pseudotuberculosis mutations that increased c-di-GMP levels and enabled biofilm development in the flea did not change the expression levels of the hms genes responsible for the synthesis and export of the extracellular polysaccharide matrix required for mature biofilm formation. The Y. pseudotuberculosis mutant uniquely expressed much higher levels of Yersinia type VI secretion system 4 (T6SS-4) in the flea, and this locus was required for flea blockage by Y. pseudotuberculosis but not for blockage by Y. pestis. Significant differences between the two species in expression of several metabolism genes, the Psa fimbrial genes, quorum sensing-related genes, transcription regulation genes, and stress response genes were evident during flea infection. IMPORTANCE Y. pestis emerged as a highly virulent, arthropod-transmitted pathogen on the basis of relatively few and discrete genetic changes from Y. pseudotuberculosis. Parallel comparisons of the in vitro and in vivo transcriptomes of Y. pestis and two Y. pseudotuberculosis variants that produce a nontransmissible infection and a transmissible infection of the flea vector, respectively, provided insights into how Y. pestis has adapted to life in its flea vector and point to evolutionary changes in the regulation of metabolic and biofilm development pathways in these two closely related species.

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Yersinia pestis autoagglutination factor is a component of the type six secretion system

Cited by 11 publications

References 50 publications

Type VI Secretion Systems Present New Insights on Pathogenic Yersinia

Type VI Secretion Systems Present New Insights on Pathogenic Yersinia

Evaluation of the roles played by Hcp and VgrG type 6 secretion system effectors in Aeromonas hydrophila SSU pathogenesis

Differential Gene Expression Patterns of Yersinia pestis and Yersinia pseudotuberculosis during Infection and Biofilm Formation in the Flea Digestive Tract

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