Role of Yersinia Murine Toxin in Survival of
            <i>Yersinia pestis</i>
            in the Midgut of the Flea Vector

Hinnebusch, B. Joseph; Rudolph, Amy E.; Cherepanov, Peter; Dixon, Jack E.; Schwan, Tom G.; Försberg, Åke

doi:10.1126/science.1069972

Cited by 277 publications

(281 citation statements)

References 20 publications

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“…It is known that HmsT is a positive regulator of the hmsHFRS operon in Y. pestis, and homologues of HmsF and HmsR are required for the synthesis of polysaccharide components of biofilms of Staphylococcus epidermidis (Gerke et al, 1998). We have also identified a Y. pseudotuberculosis YPIII pIB1 hms gene (hmsF; The murine lethal toxin (phospholipase D) encoded on the 100 kb plasmid pMT1 in Y. pestis also plays a role in the survival of Y. pestis in the midgut of fleas (Hinnebusch et al, 2002). However, pMT1 does not appear to be important for infection of C. elegans since the Y. pestis Java-9 strain that lacks this plasmid (confirmed by DNA microarray analysis; S. J. Hinchliffe & B. W. Wren, unpublished data) readily caused biofilms.…”

Section: Discussionmentioning

confidence: 99%

A Caenorhabditis elegans model of Yersinia infection: biofilm formation on a biotic surface

et al. 2003

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To investigate Yersinia pathogenicity and the evolutionary divergence of the genus, the effect of pathogenic yersiniae on the model organism Caenorhabditis elegans was studied. Three strains of Yersinia pestis, including a strain lacking pMT1, caused blockage and death of C. elegans; one strain, lacking the haemin storage (hms) locus, caused no effect. Similarly, 15 strains of Yersinia enterocolitica caused no effect. Strains of Yersinia pseudotuberculosis showed different levels of pathogenicity. The majority of strains (76 %) caused no discernible effect; 5 % caused a weak infection, 9?5 % an intermediate infection, and 9?5 % a severe infection. There was no consistent relationship between serotype and severity of infection; nor was there any relationship between strains causing infection of C. elegans and those able to form a biofilm on an abiotic surface. Electron microscope and cytochemical examination of infected worms indicated that the infection phenotype is a result of biofilm formation on the head of the worm. Seven transposon mutants of Y. pseudotuberculosis strain YPIII pIB1 were completely or partially attenuated; mutated genes included genes encoding proteins involved in haemin storage and lipopolysaccharide biosynthesis. A screen of 15 defined C. elegans mutants identified four where mutation caused (complete) resistance to infection by Y. pseudotuberculosis YPIII pIB1. These mutants, srf-2, srf-3, srf-5 and the dauer pathway gene daf-1, also exhibit altered binding of lectins to the nematode surface. This suggests that biofilm formation on a biotic surface is an interactive process involving both bacterial and invertebrate control mechanisms.

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Section: Discussionmentioning

confidence: 99%

A Caenorhabditis elegans model of Yersinia infection: biofilm formation on a biotic surface

et al. 2003

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“…The ymt gene encoding for a phospholipase D in Yersinia pestis, for example, is needed for persistence in the flea midgut (Hinnebusch et al, 2002). Phospholipase C produced by Mycobacterium abscessus is crucial for survival in amoeba and is suggested to cause damage to mouse macrophages presumably by hydrolysis of membrane phospholipids (N'goma et al, 2015).…”

Section: Strain Selectionmentioning

confidence: 99%

Insect pathogenicity in plant-beneficial pseudomonads: phylogenetic distribution and comparative genomics

et al. 2016

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Bacteria of the genus Pseudomonas occupy diverse environments. The Pseudomonas fluorescens group is particularly well-known for its plant-beneficial properties including pathogen suppression. Recent observations that some strains of this group also cause lethal infections in insect larvae, however, point to a more versatile ecology of these bacteria. We show that 26 P. fluorescens group strains, isolated from three continents and covering three phylogenetically distinct sub-clades, exhibited different activities toward lepidopteran larvae, ranging from lethal to avirulent. All strains of sub-clade 1, which includes Pseudomonas chlororaphis and Pseudomonas protegens, were highly insecticidal regardless of their origin (animals, plants). Comparative genomics revealed that strains in this sub-clade possess specific traits allowing a switch between plant-and insect-associated lifestyles. We identified 90 genes unique to all highly insecticidal strains (sub-clade 1) and 117 genes common to all strains of sub-clade 1 and present in some moderately insecticidal strains of sub-clade 3. Mutational analysis of selected genes revealed the importance of chitinase C and phospholipase C in insect pathogenicity. The study provides insight into the genetic basis and phylogenetic distribution of traits defining insecticidal activity in plant-beneficial pseudomonads. Strains with potent dual activity against plant pathogens and herbivorous insects have great potential for use in integrated pest management for crops.

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“…For instance, the ymt gene located on the pFra plasmid encodes phospholipase D, which enhances the ability of Y. pestis to colonize the flea midgut (Hinnebusch et al 2002). The pFra plasmid also carries the caf1M1A1 operon, which encodes a protein capsule that is required for infection of mice by the flea-borne route (Sebbane et al 2009).…”

Section: Lateral Gene Transfermentioning

confidence: 99%

Host Specificity of Bacterial Pathogens

Bäumler

Fang

2013

Cold Spring Harbor Perspectives in Medicine

173

134

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Role of Yersinia Murine Toxin in Survival of Yersinia pestis in the Midgut of the Flea Vector

Cited by 277 publications

References 20 publications

A Caenorhabditis elegans model of Yersinia infection: biofilm formation on a biotic surface

A Caenorhabditis elegans model of Yersinia infection: biofilm formation on a biotic surface

Insect pathogenicity in plant-beneficial pseudomonads: phylogenetic distribution and comparative genomics

Host Specificity of Bacterial Pathogens

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