Loss of a Biofilm-Inhibiting Glycosyl Hydrolase during the Emergence of
            <i>Yersinia pestis</i>

Erickson, David L.; Jarrett, Clayton O.; Callison, Julie; Fischer, Elizabeth R.; Hinnebusch, B. Joseph

doi:10.1128/jb.01181-08

Cited by 50 publications

(60 citation statements)

References 51 publications

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“…The ability of Y. pestis to form a biofilm, both in the flea and in vitro, depends on the hms gene products encoded in the Pgm locus, which synthesize the ␤-1,6 N-acetyl-D-glucosamine polysaccharide component of the extracellular matrix of the biofilm (32,41,43,54,59,60). The Pgm-dependent biofilm is produced only KIM6ϩ in logarithmic-phase (log) and stationary-phase (stat) cultures grown at 21 or 37°C in media containing high (ϩ) or low (Ϫ) Mg 2ϩ (A) and in fleas 3 h and 2 weeks after infection (B) were determined by quantitative RT-PCR.…”

Section: Discussionmentioning

confidence: 99%

Induction of the Yersinia pestis PhoP-PhoQ Regulatory System in the Flea and Its Role in Producing a Transmissible Infection

et al. 2013

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cTransmission of Yersinia pestis is greatly enhanced after it forms a bacterial biofilm in the foregut of the flea vector that interferes with normal blood feeding. Here we report that the ability to produce a normal foregut-blocking infection depends on induction of the Y. pestis PhoP-PhoQ two-component regulatory system in the flea. Y. pestis phoP-negative mutants achieved normal infection rates and bacterial loads in the flea midgut but produced a less cohesive biofilm both in vitro and in the flea and had a greatly reduced ability to localize to and block the flea foregut. Thus, not only is the PhoP-PhoQ system induced in the flea gut environment, but also this induction is required to produce a normal transmissible infection. The altered biofilm phenotype in the flea was not due to lack of PhoPQ-dependent or PmrAB-dependent addition of aminoarabinose to the Y. pestis lipid A, because an aminoarabinose-deficient mutant that is highly sensitive to cationic antimicrobial peptides had a normal phenotype in the flea digestive tract. In addition to enhancing transmissibility, induction of the PhoP-PhoQ system in the arthropod vector prior to transmission may preadapt Y. pestis to resist the initial encounter with the mammalian innate immune response.

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Section: Discussionmentioning

confidence: 99%

Induction of the Yersinia pestis PhoP-PhoQ Regulatory System in the Flea and Its Role in Producing a Transmissible Infection

et al. 2013

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“…Acquisition of the hms locus predates the evolutionary divergence of Y. pestis from Y. pseudotuberculosis (22). However, Y. pseudotuberculosis, but not Y. pestis, expresses nghA, which encodes a PNAG hydrolase that is thought to interfere with biofilm formation in the flea gut (21,23). Of note, Y. pseudotuberculosis infection of fleas triggers intestinal toxicity and diarrhea in X. cheopis (24).…”

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confidence: 99%

“…blockade, and regurgitative transmission (6); the locus comprises a four-gene operon (hmsHFRS) for the synthesis of poly-(␤1-6)-N-acetylglucosamine (PNAG), an extracellular matrix polymer of Y. pestis biofilms (20,21). Acquisition of the hms locus predates the evolutionary divergence of Y. pestis from Y. pseudotuberculosis (22).…”

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YfbA, a Yersinia pestis Regulator Required for Colonization and Biofilm Formation in the Gut of Cat Fleas

et al. 2014

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For transmission to new hosts, Yersinia pestis, the causative agent of plague, replicates as biofilm in the foregut of fleas that feed on plague-infected animals or humans. Y. pestis biofilm formation has been studied in the rat flea; however, little is known about the cat flea, a species that may bridge zoonotic and anthroponotic plague cycles. Here, we show that Y. pestis infects and replicates as a biofilm in the foregut of cat fleas in a manner requiring hmsFR, two determinants for extracellular biofilm matrix. Examining a library of transposon insertion mutants, we identified the LysR-type transcriptional regulator YfbA, which is essential for Y. pestis colonization and biofilm formation in cat fleas.

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“…Among important bacterial pathogens, PNAG is known to be produced by S. aureus and Staphylococcus epidermidis (23,25,26), E. coli (13,42), Bordetella pertussis and Bordetella parapertussis (29,36), Aggregatibacter actinomycetemcomitans (15), Acinetobacter spp. (8), and Yersinia pestis (10,12). Based on genetic homology, loci likely encoding PNAG biosynthetic proteins are found in Burkholderia cenocepacia and Klebsiella pneumoniae.…”

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Synthetic β-(1→6)-Linked N-Acetylated and Nonacetylated Oligoglucosamines Used To Produce Conjugate Vaccines for Bacterial Pathogens

et al. 2010

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Vaccines for pathogens usually target strain-specific surface antigens or toxins, and rarely is there broad antigenic specificity extending across multiple species. Protective antibodies for bacteria are usually specific for surface or capsular antigens. ␤-(136)-Poly-N-acetyl-D-glucosamine (PNAG) is a surface polysaccharide produced by many pathogens, including Staphylococcus aureus, Escherichia coli, Yersinia pestis, Bordetella pertussis, Acinetobacter baumannii, and others. Protective antibodies to PNAG are elicited when a deacetylated glycoform (deacetylated PNAG [dPNAG]; <30% acetate) is used in conjugate vaccines, whereas highly acetylated PNAG does not induce such antibodies. Chemical derivation of dPNAG from native PNAG is imprecise, so we synthesized both ␤-(136)-D-glucosamine (GlcNH 2 ) and ␤-(136)-D-N-acetylglucosamine (GlcNAc) oligosaccharides with linkers on the reducing termini that could be activated to produce sulfhydryl groups for conjugation to bromoacetyl groups introduced onto carrier proteins. Synthetic 5-mer GlcNH 2 (5GlcNH 2 ) or 9GlcNH 2 conjugated to tetanus toxoid (TT) elicited mouse antibodies that mediated opsonic killing of multiple S. aureus strains, while the antibodies that were produced in response to 5GlcNAc-or 9GlcNAc-TT did not mediate opsonic killing. Rabbit antibodies to 9GlcNH 2 -TT bound to PNAG and dPNAG antigens, mediated killing of S. aureus and E. coli, and protected against S. aureus skin abscesses and lethal E. coli peritonitis.

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Loss of a Biofilm-Inhibiting Glycosyl Hydrolase during the Emergence of Yersinia pestis

Cited by 50 publications

References 51 publications

Induction of the Yersinia pestis PhoP-PhoQ Regulatory System in the Flea and Its Role in Producing a Transmissible Infection

Induction of the Yersinia pestis PhoP-PhoQ Regulatory System in the Flea and Its Role in Producing a Transmissible Infection

YfbA, a Yersinia pestis Regulator Required for Colonization and Biofilm Formation in the Gut of Cat Fleas

Synthetic β-(1→6)-Linked N-Acetylated and Nonacetylated Oligoglucosamines Used To Produce Conjugate Vaccines for Bacterial Pathogens

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