ライフサイエンスコーパス: pestis

1 uropean Black Death/bubonic plague (Yersinia pestis).

2 al stability of the chaperone LcrH (Yersinia pestis).

3 eadly respiratory disease caused by Yersinia pestis.

4 ghtly controlled virulence determinant of Y. pestis.

5 Hfq in the closely related species Yersinia pestis.

6 ense in mice challenged intranasally with Y. pestis.

7 samine to the lipooligosaccharide core of Y. pestis.

8 infection kinetics and early clearance of Y. pestis.

9 LpxE does not attenuate the virulence of Y. pestis.

10 rfaH in Y. pseudotuberculosis but not in Y. pestis.

11 tential agents of bioterrorism, including Y. pestis.

12 eudotuberculosis, while yapJ is unique to Y. pestis.

13 tified Ilp as a novel virulence factor of Y. pestis.

14 res the virulence defects of nonpigmented Y. pestis.

15 tor in evolution of the high virulence of Y. pestis.

16 rticipate in broadening the host range of Y. pestis.

17 ague strains are basal to all known Yersinia pestis.

18 equences, of which the majority are Yersinia pestis.

19 hoQ system, OmpR-EnvZ was the only one of Y. pestis' 23 other 2CSs required for production of bubonic

20 nding and delivery of Yops (cytotoxins of Y. pestis), a novel interaction, distinct from other bacter

21 Plague is initiated by Yersinia pestis, a highly virulent bacterial pathogen.

22 more, following intranasal infection with Y. pestis, A2AP-deficient mice exhibit no difference in sur

23 studied the interaction between the Yersinia pestis ABC heme importer (HmuUV) and its partner substra

24 Deletion of ivy decreased Y. pestis' ability to counter lysozyme and polymorphonuclea

25 The Yersinia pestis adhesin molecule Ail interacts with the extracell

26 Yersinia pestis adopts a unique life stage in the digestive tract

27 uence of a singular introduction of Yersinia pestis, after which the disease established itself in Eu

28 These findings demonstrate that Y. pestis Ail uses multiple extracellular loops to interact

29 ble in <4 h for B. anthracis and <6 h for Y. pestis and B. pseudomallei One exception was B. pseudoma

30 potential bioterrorism agents like Yersinia pestis and Bacillus anthracis which feature on the Cente

31 ame species, including 5 strains of Yersinia pestis and Bacillus anthracis.

32 r displayed 100% (n = 59) inclusivity for Y. pestis and consistent intraspecific signal transduction

33 irst global analysis of AI-2 signaling in Y. pestis and identifies potential roles for the system in

34 This response was not specific to Y. pestis and involved a reduced sensitivity to M2 polariza

35 0 nM between EGFP-labeled LcrV from Yersinia pestis and its cognate membrane-bound protein YopB inser

36 kines important to host responses against Y. pestis and many other infectious agents.

37 atform for intranasal vaccination against Y. pestis and other infectious pathogens.

38 ical drug target for infections caused by Y. pestis and possibly for those caused by other blood-born

39 teins based on the roles of their aligned Y. pestis and S. enterica partners and showed that up to 73

40 igmentation locus-negative (pgm(-)) Yersinia pestis and that this phenotype maps to a 30-centimorgan

41 bacterial spread is key to understanding Y. pestis and the immune responses it encounters during inf

42 e protective F1 capsular antigen of Yersinia pestis and the LcrV protein required for secretion of vi

43 ication of new virulence factors in Yersinia pestis and understanding their molecular mechanisms duri

44 Studies in Y. pestis and Y. pseudotuberculosis have shown that YopM su

45 nclude homologous sequences from numerous Y. pestis and Y. pseudotuberculosis strains, we determined

46 that omptin cleavage is specific for the Y. pestis and Y. pseudotuberculosis YapE orthologues but is

47 e in a strain-specific manner and only in Y. pestis and Y. pseudotuberculosis.

48 erences in virulence genes found in Yersinia pestis and Yersinia pseudotuberculosis compared to other

49 J-dependent cytotoxicity induced by Yersinia pestis and Yersinia pseudotuberculosis paradoxically lea

50 Flea-borne zoonoses such as plague (Yersinia pestis) and murine typhus (Rickettsia typhi) caused sign

51 y response induced by other lethal (Yersinia pestis) and non-lethal (Legionella pneumophila, Pseudomo

52 monella enterica serovar Typhi, and Yersinia pestis), and 3 protozoa (Leishmania spp., Plasmodium spp

53 ptibility by 50% to 75% for B. anthracis, Y. pestis, and B. pseudomallei compared to conventional met

54 n resistance in Bacillus anthracis, Yersinia pestis, and Francisella tularensis.

55 pathogen interactions of B. mallei, Yersinia pestis, and Salmonella enterica.

56 from pathogens such as Salmonella, Yersinia pestis, and the virulent Francisella tularensis subspeci

57 ogressive stages of the disease with anti-Y. pestis antibodies alone or in combination with the corti

58 ce in many bacterial pathogens, including Y. pestis, any change in autotransporter content should be

59 y on the surface of many mammalian cells, Y. pestis appears to prefer interacting with certain types

60 unded fears of the intentional release of Y. pestis as a biological weapon.

61 t steps in the evolution and emergence of Y. pestis as a flea-borne pathogen.

62 luding the plague causing bacterium Yersinia pestis, avoid activating this pathway to enhance their v

63 ther Yersinia pseudotuberculosis or Yersinia pestis bacteria express the small RNAs YSR35 or YSP8, wi

64 Y. pestis biofilm formation has been studied in the rat fle

65 cyclic diguanylate is essential for Yersinia pestis biofilm formation that is important for blockage-

66 of medium peptides associated with Yersinia pestis biomass and improve the quality of proteomic meas

67 9th century intestinal specimen and Yersinia pestis ("Black Death" plague) in a medieval tooth, which

68 also show that cleavage of YapE occurs in Y. pestis but not in the enteric Yersinia species, and requ

69 Wild-type Y. pestis, but not a Pla mutant (Deltapla), degrades FasL,

70 ved from the recognition of intracellular Y. pestis by host Toll-like receptor 7 (TLR7).

71 The Gram-negative bacteria Yersinia pestis, causative agent of plague, is extremely virulent

72 The 14th-18th century pandemic of Yersinia pestis caused devastating disease outbreaks in Europe fo

73 enomes from Southern Siberia suggest that Y. pestis caused some form of disease in humans prior to th

74 Yersinia pestis causes bubonic plague, a fulminant disease where

75 Yersinia pestis causes bubonic, pneumonic, and septicemic plague,

76 The Gram-negative bacterium Yersinia pestis causes plague, a rapidly progressing and often fa

77 Yersinia pestis causes the fatal respiratory disease pneumonic pl

78 endent caspase-1 activation pathway after Y. pestis challenge.

79 uantitate the internalization of virulent Y. pestis CO92 by macrophages and the subsequent activation

80 poprotein (Lpp) and MsbB attenuated Yersinia pestis CO92 in mouse and rat models of bubonic and pneum

81 haride function, reduced the virulence of Y. pestis CO92 in mouse models of bubonic and pneumonic pla

82 msbB double mutant of the highly virulent Y. pestis CO92 strain.

83 ltamsbB double mutant severely attenuated Y. pestis CO92 to evoke pneumonic plague in a mouse model w

84 ogen-activating protease (pla) genes from Y. pestis CO92.

85 subcutaneous infection with the virulent Y. pestis CO92.

86 al regulator YfbA, which is essential for Y. pestis colonization and biofilm formation in cat fleas.

87 The pH 6 antigen (Psa) of Yersinia pestis consists of fimbriae that bind to two receptors:

88 Importantly, we find that Y. pestis containing combined deletions of YopJ and YopM in

89 Y. pestis CU pathways y0348-0352 and y1858-1862 were found

90 e rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effecto

91 The Y. pestis derivative strain lacking the nhaA and nhaB genes

92 A fast and efficient Y. pestis dissemination in SEG mice may be critical for the

93 nd water-borne enteric species from which Y. pestis diverged less than 6,400 y ago, exhibits signific

94 Here, we show that Y. pestis does not appreciably cleave A2AP in a Pla-depende

95 ty to the flea vectors of plague, whereas Y. pestis does not.

96 st severe form of disease caused by Yersinia pestis due to its ease of transmission, rapid progressio

97 formation and acquisition and fitness of Y. pestis during flea gut infection, consistent with posttr

98 t a step-wise evolutionary model in which Y. pestis emerged as a flea-borne clone, with each genetic

99 ich require help from fibrin to withstand Y. pestis encounters and effectively clear bacteria.

100 response to Y. pestis infection, and that Y. pestis entry into macrophages may involve the participat

101 detrimental effect under proper control, Y. pestis expresses the caf operon (encoding the F1 capsule

102 antibodies blocked type III injection by Y. pestis expressing lcrV(W22703) or lcrV(WA-314) and prote

103 ignificant effect on transcription of the Y. pestis feo promoter.

104 Under static growth conditions, the Y. pestis feo::lacZ fusion was repressed by iron in a Fur-d

105 The emergence of Y. pestis fits evolutionary theories that emphasize ecologi

106 entified has not been found in any extant Y. pestis foci sampled to date, and has its ancestry in str

107 opJ, yopM, and yopJ yopM mutants ofY ersinia pestis Following intravenous infection of mice, theY.

108 m BT organisms (Bacillus anthracis, Yersinia pestis, Francisella tularensis, Brucella spp., Burkholde

109 inct strains of Bacillus anthracis, Yersinia pestis, Francisella tularensis, Burkholderia mallei, Bur

110 daptation that followed the divergence of Y. pestis from the closely related food- and waterborne ent

111 isition of pPCP1 during the divergence of Y. pestis from Y. pseudotuberculosis, and are the first evi

112 As Y. pestis further evolved, modern strains acquired a single

113 s; however, it is not known at what point Y. pestis gained the ability to induce a fulminant pneumoni

114 The Y. pestis genome contains additional CU pathways that are c

115 Here we present five Y. pestis genomes from one of the last European outbreaks o

116 Here, we present six new European Y. pestis genomes spanning the Late Neolithic to the Bronze

117 variety of pathogenic bacteria including Y. pestis, H. influenzae, and Proteus that cause plague, me

118 e motility, the role of quorum sensing in Y. pestis has been unclear.

119 Yersinia pestis has caused at least three human plague pandemics.

120 Because Yersinia pestis HasA (HasA(yp)) presents a Gln at position 32, we

121 eport the oldest direct evidence of Yersinia pestis identified by ancient DNA in human teeth from Asi

122 mice that are cleaved and/or processed by Y. pestis in a Pla-dependent manner.

123 nfluenza A in lesser snow geese and Yersinia pestis in coyotes), we argue that with careful experimen

124 n alone had no effect on the virulence of Y. pestis in either bubonic or pneumonic plague models.

125 regulates the entry and survival of Yersinia pestis in host macrophages is poorly understood.

126 apacity to modulate binding properties of Y. pestis in its hosts, in conjunction with other adhesins.

127 no significant reduction in virulence of Y. pestis in mice when it was administered i.n. but actuall

128 The discovery of molecular signatures of Y. pestis in prehistoric Eurasian individuals and two genom

129 PhiA1122::luxAB rapidly detects Y. pestis in pure culture and human serum by transducing a

130 , we report the first direct detection of Y. pestis in soil, which could be extremely useful in confi

131 re), sensitive, and specific detection of Y. pestis in such complex samples.

132 Growth restriction of Yersinia pestis in the absence of calcium (low-calcium response [

133 port is indispensable for the survival of Y. pestis in the bloodstreams of infected animals and thus

134 iron(III)-yersiniabactin import in Yersinia pestis In this study, we compared the impact of ybtPQ on

135 s of C57BL/6 and SEG MPs exposed to Yersinia pestis in vitro were examined.

136 kine response, and a higher resistance to Y. pestis-induced apoptosis.

137 single-nucleotide polymorphisms modulate Y. pestis-induced cytokine responses.

138 host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as

139 g that a noncanonical mechanism occurs in Y. pestis-infected macrophages.

140 erferon (IFN) signaling is induced during Y. pestis infection and contributes to neutrophil depletion

141 ntributes to type I IFN expression during Y. pestis infection and suggest that the TLR7-driven type I

142 A hallmark of Yersinia pestis infection is a delayed inflammatory response earl

143 vivo; the role of A2AP during respiratory Y. pestis infection is not known either.

144 The formation of fibrin at sites of Y. pestis infection supports innate host defense against pl

145 lling IL-18 and IL-1beta production after Y. pestis infection, and NLRP12-deficient mice were more su

146 s for NF-kappaB activation in response to Y. pestis infection, and that Y. pestis entry into macropha

147 e conclude that, throughout the course of Y. pestis infection, OmpR-EnvZ is required to counter toxic

148 ct with YopD within targeted cells during Y. pestis infection, suggesting that YopK's regulatory mech

149 Using established mouse models of Y. pestis infection, we demonstrated that despite the high

150 agonist), E. coli LPS (a TLR4 agonist) or Y. pestis infection, while the PI3K and PKC inhibitors were

151 odes (LNs), or buboes, characterize Yersinia pestis infection, yet how they form and function is unkn

152 ome activation, and host resistance after Y. pestis infection.

153 nd PKC inhibitors were selective only for Y. pestis infection.

154 ndant roles for yapJ and yapK in systemic Y. pestis infection.

155 yapJ in its contribution to disseminated Y. pestis infection.

156 for pneumonic plague during outbreaks of Y. pestis infections.

157 Here, we show that Y. pestis infects and replicates as a biofilm in the foregu

158 ptotic death pathway after infection with Y. pestis, influenced by Toll-like receptor 4-TIR-domain-co

159 cularly the N terminus of YscF from Yersinia pestis, influences host immune responses.

160 repeated emergence of diverse lineages of Y pestis into human populations.

161 Here we show that in Yersinia pestis, irp2, a gene encoding the synthetase (HMWP2) for

162 Yersinia pestis is a Gram-negative bacterium that is the causativ

163 Yersinia pestis is a tier 1 agent due to its contagious pneumopat

164 Yersinia pestis is an arthropod-borne bacterial pathogen that evo

165 The plasminogen activator (Pla) of Yersinia pestis is an omptin family member that is very important

166 Transmission of Yersinia pestis is greatly enhanced after it forms a bacterial bi

167 s frenzied inflammatory response to Yersinia pestis is poorly understood.

168 Yersinia pestis is the causative agent of bubonic and pneumonic p

169 Yersinia pestis is the causative agent of plague.

170 The bacteria Yersinia pestis is the etiological agent of plague and has caused

171 The plague bacillus Yersinia pestis is unique among the pathogenic Enterobacteriaceae

172 used by the Gram-negative bacterium Yersinia pestis, is favored by a robust early innate immune respo

173 l or monoclonal antibodies raised against Y. pestis KIM D27 LcrV (LcrV(D27)) bind LcrV from Y. entero

174 crV gene on the pCD1 virulence plasmid of Y. pestis KIM D27 with either lcrV(W22703) or lcrV(WA-314)

175 This study focuses on the Y. pestis KIM yapV gene and its product, recognized as an a

176 ltures of two attenuated strains of Yersinia pestis [KIM D27 (pgm-) and KIM D1 (lcr-)] grown in sever

177 Additionally, LpxE synthesis in wild-type Y. pestis KIM6+(pCD1Ap) led to slight attenuation by s.c. i

178 lethal doses (LD50) (2.4 x 10(4) CFU) of Y. pestis KIM6+(pCD1Ap) than chi10057(pYA3332) (40% surviva

179 confirmed when they were overexpressed in Y. pestis KIM6+.

180 ants of Y. pseudotuberculosis IP32953 and Y. pestis KIM6+.

181 Y. pestis lacking Ivy had attenuated virulence, unless anim

182 In vivo, Y. pestis lacking OmpR-EnvZ did not induce an early immune

183 the ear with wild-type (WT) or attenuated Y. pestis lacking the pYV virulence plasmid (pYV(-)).

184 We report that Yersinia pestis LcrF binds to and activates transcription of ExsA

185 that plasmid-expressed ExsA complements a Y. pestis lcrF mutant for T3SS gene expression.

186 agged influenza hemagglutinin 5 and Yersinia pestis LcrV antigens.

187 We find the origins of the Yersinia pestis lineage to be at least two times older than previ

188 We conclude that the Y pestis lineages that caused the Plague of Justinian and

189 pendent addition of aminoarabinose to the Y. pestis lipid A, because an aminoarabinose-deficient muta

190 Thus, by degrading FasL, Y. pestis manipulates host cell death pathways to facilitat

191 ss the functional role of AI-2 sensing in Y. pestis, microarray studies were conducted by comparing D

192 produce disease, the causal agent (Yersinia pestis) must rapidly sense and respond to rapid variatio

193 haB in trans restored the survival of the Y. pestis nhaA nhaB double deletion mutant in blood.

194 we sequenced and analysed draft genomes of Y pestis obtained from two individuals who died in the fir

195 agents such as Bacillus anthracis, Yersinia pestis, or Burkholderia pseudomallei Conventional suscep

196 shown with recombinant Escherichia coli, Y. pestis, or purified passenger domains.

197 a functional ureD was sufficient to make Y. pestis orally toxic to fleas.

198 Thus, Y. pestis-orchestrated LN remodeling promoted its dissemina

199 The Y. pestis outer membrane Pla protease is essential for the

200 flammatory responses and enables enhanced Y. pestis outgrowth in the lungs.

201 ith host sensing of YscF, consistent with Y. pestis pathogenesis.

202 adly used in many fields, including Yersinia pestis pathogenesis.

203 h could be extremely useful in confirming Y. pestis persistence in the ground.

204 Recently, a Y. pestis pgm strain was isolated from a researcher with he

205 eloped lethal plague when challenged with Y. pestis pgm strains.

206 Y. pestis phoP-negative mutants achieved normal infection r

207 ing infection depends on induction of the Y. pestis PhoP-PhoQ two-component regulatory system in the

208 a single putatively extinct clade in the Y. pestis phylogeny.

209 fection with either wild-type or Deltapla Y. pestis, Prdx6-deficient mice exhibit no differences in b

210 rough tight regulation of the caf operon, Y. pestis precisely balances its capsular anti-phagocytic p

211 gests that both Y. pseudotuberculosis and Y. pestis produce an oligosaccharide core with a single O-a

212 n to the 2' position of lipid A, in Yersinia pestis produced bisphosphoryl hexa-acylated lipid A at 3

213 Yersinia pestis produces and secretes a toxin named pesticin that

214 on of a single protein, e.g., YscF (Yersinia pestis), PscF (Pseudomonas aeruginosa), PrgI (Salmonella

215 ptional profiling experiments to identify Y. pestis quorum sensing regulated functions.

216 Y. pestis recently evolved from the gastrointestinal pathog

217 n, we found that infection with wild-type Y. pestis reduces the abundance of extracellular Prdx6 in t

218 Inhalation of the bacterium Yersinia pestis results in primary pneumonic plague.

219 etiologic agent of bubonic plague, Yersinia pestis, senses self-produced, secreted chemical signals

220 , lungs of mice challenged with wild-type Y. pestis show reduced levels of FasL and activated caspase

221 osis, the relatively recent progenitor of Y. pestis, shows no similar trans-complementation effect, w

222 ivity of a DABA DC homologue from a Yersinia pestis siderophore biosynthetic pathway.

223 In Yersinia pestis, single mutations in either yfe or feo result in

224 eened DNA extracts for the presence of the Y pestis-specific pla gene on the pPCP1 plasmid using prim

225 ivator protease), which is encoded on the Y. pestis-specific plasmid pPCP1.

226 e relevant protein markers encoded by the Y. pestis-specific plasmids pFra (murine toxin) and pPla (p

227 recent 19(th) century pandemic, in which Y. pestis spread worldwide [5] and became endemic in severa

228 al. (2014) explore the mechanism by which Y. pestis spreads and thus leads to this striking lymphaden

229 Through deep sequencing analysis of the Y. pestis sRNA-ome, we found 63 previously unidentified put

230 utaneously infected with a fully virulent Y. pestis strain and treated at progressive stages of the d

231 nic approach, we created 5,088 mutants of Y. pestis strain CO92 and screened them in a mouse model of

232 ction against subcutaneous challenge with Y. pestis strain CO92 even though it fails to protect mice

233 day prior to lethal pulmonary exposure to Y. pestis strain KIM D27 significantly improves survival of

234 The YPTB3286-like gene of most Y. pestis strains appears to be inactivated, perhaps in fav

235 Y. pestis strains containing deletions in CU pathways y0348

236 d them with a database of genomes from 131 Y pestis strains from the second and third pandemics, and

237 A phylogenic tree including 36 Y. pestis strains highlighted an association between the ge

238 Deletion mutants of ilp were generated in Y. pestis strains KIM5(pCD1(+)) Pgm(-) (pigmentation negati

239 Yersinia pestis virulence and found that Y. pestis strains lacking the major Na(+)/H(+) antiporters,

240 onstructed draft genomes of the infectious Y pestis strains, compared them with a database of genomes

241 All Y. pestis strains, including those phylogenetically closest

242 red to that after infection with Deltapla Y. pestis, suggesting that Pla cleaves Prdx6 in the pulmona

243 and oxidative stress genes that may help Y. pestis survive at the host temperature.

244 atory responses through TLRs by the Yersinia pestis T3S needle protein, YscF, the Salmonella enterica

245 s binding sites in both P. aeruginosa and Y. pestis T3SS promoters prevent activation by ExsA and Lcr

246 In Yersinia pestis the autotransporter YapE has adhesive properties

247 Yersinia pestis (the plague bacillus) and its ancestor, Yersinia

248 Pathogenic Yersinia, including Y. pestis, the agent of plague in humans, and Y. pseudotube

249 oducts are functional receptors for Yersinia pestis, the agent of plague, as shown by overexpression

250 thropod-borne transmission route of Yersinia pestis, the bacterial agent of plague, is a recent evolu

251 Yersina pestis, the bubonic plague bacterium, is coated with a p

252 is no FDA-approved vaccine against Yersinia pestis, the causative agent of bubonic and pneumonic pla

253 Yersinia pestis, the causative agent of plague, binds host cells

254 Yersinia pestis, the causative agent of plague, evolved from the

255 Yersinia pestis, the causative agent of plague, expresses the pla

256 nguish DNA amplicons generated from Yersinia pestis, the causative agent of plague, from the closely

257 Yersinia pestis, the causative agent of plague, is able to suppre

258 For transmission to new hosts, Yersinia pestis, the causative agent of plague, replicates as bio

259 Yersinia pestis, the causative agent of plague, uses a type III s

260 Yersinia pestis, the causative agent of plague, utilizes a type I

261 al gene prediction in the bacterium Yersinia pestis, the causative agent of plague.

262 racterization of the AI-2 system in Yersinia pestis, the causative agent of plague.

263 a candidate recombinant antigen for Yersinia pestis, the causative agent of plague.

264 is essential in the pathogenesis of Yersinia pestis, the causative agent of plague.

265 Yersinia pestis, the cause of the disease plague, forms biofilms

266 Yersinia pestis, the etiologic agent of plague, is a bacterium as

267 agonist, confers protection against Yersinia pestis, the etiologic agent of plague.

268 possible scenario for the early spread of Y. pestis: the pathogen may have entered Europe from Centra

269 most ancestral, deeply rooted strains of Y. pestis to cause pneumonic plague, indicating that Y. pes

270 c basis of the evolutionary adaptation of Y. pestis to flea-borne transmission.

271 vector prior to transmission may preadapt Y. pestis to resist the initial encounter with the mammalia

272 s, suggesting an evolutionary adaption of Y. pestis to specific local animal hosts or reservoirs.

273 These findings reveal adaptations of Y. pestis to the dermis and how these adaptations can defin

274 m for interrogating such couplings: Yersinia pestis transmission exerts intense selective pressure dr

275 ) mice with a subunit vaccine that blocks Y. pestis type III secretion generated protection against p

276 Y. pestis type III secretion system effectors YopJ and YopM

277 During infection, Yersinia pestis uses its F1 capsule to enhance survival and cause

278 rine/threonine kinase YopO (YpkA in Yersinia pestis), uses monomeric actin as bait to recruit and pho

279 The development of live, attenuated Y. pestis vaccines may be facilitated by detoxification of

280 ible role of Na(+)/H(+) antiport in Yersinia pestis virulence and found that Y. pestis strains lackin

281 emonstrated a role played by Lpp in Yersinia pestis virulence in mouse models of bubonic and pneumoni

282 One mechanism contributing to Y. pestis virulence is the presence of a type-three secreti

283 These findings indicate that Y. pestis was capable of causing pneumonic plague before it

284 In addition, Y. pestis was identified directly from positive blood cultu

285 , ureD mutation early in the evolution of Y. pestis was likely subject to strong positive selection b

286 o cause pneumonic plague, indicating that Y. pestis was primed to infect the lungs at a very early st

287 ication of YapE appears to be specific to Y. pestis, was acquired along with the acquisition of pPCP1

288 d to the LcrV virulence factor from Yersinia pestis were characterised for their Fab affinity against

289 ludes serious pathogens such as the Yersinia pestis, which causes plague, Yersinia pseudotuberculosis

290 Thus, the interactions of Y. pestis with its flea vector that lead to colonization an

291 immune environment leading to survival of Y. pestis within the eukaryotic host.

292 e, we demonstrate that omptin cleavage of Y. pestis YapE is required to mediate bacterial aggregation

293 Yersinia pestis YapV is homologous to Shigella flexneri IcsA, and

294 However, some non-pestis Yersinia strains and Enterobacteriaceae did elici

295 ase, LpxE, from Francisella tularensis in Y. pestis yields predominantly 1-dephosphorylated lipid A,

296 Shigella flexneri OspF protein and Yersinia pestis YopH protein, to rewire kinase-mediated responses

297 Thus, we conclude that Y. pestis YopJ and YopM can both exert a tight control of h

298 of IgG response to whole-cell lysates of Y. pestis (YpL) and subunit LcrV similar to those seen with

299 ture, blocking effector transport even in Y. pestis yscF variants that are otherwise calcium blind, a

300 ases: Burkholderia mallei BmaI1 and Yersinia pestis YspI.