ライフサイエンスコーパス: T3SS

1 T3SS are phylogenetically divided into several families

2 T3SS bistability is reversible, indicating a non-genetic

3 T3SS bistability requires the transcriptional activator

4 T3SS effectors target host innate immune mechanisms, and

5 T3SS expression is bistable in the homogeneous environme

6 T3SS-OFF bacteria showed no fitness advantage in competi

7 T3SS-OFF strains outcompeted WT PA103 in vivo, whereas a

8 T3SSs are widespread in nature and are encoded not only

9 T3SSs involved in virulence (vT3SSs) are evolutionarily

10 uch as quercetin, also inactivated the SPI-1 T3SS and attenuated S. Typhimurium invasion.

11 howed that SeoC is translocated by the SPI-1 T3SS.

12 he Salmonella pathogenicity island 1 (SPI-1) T3SS effectors SopB and SopE2.

13 rtners, and physiological functions of SPI-2 T3SS effectors in the context of the selective pressures

14 ty island 2 type III secretion system (SPI-2 T3SS), which is required to translocate at least 28 effe

15 of antigen-presenting cells results in SPI-2 T3SS-dependent ubiquitination and reduction of surface-l

16 some effectors of type 3 secretion system 3 (T3SS-3), which is also required for virulence, are expre

17 A T3SS effector, exotoxin U (ExoU), can inhibit activation

18 C) and increased intraepithelial growth in a T3SS-2-dependent manner.

19 iously, it has been reported that EPEC, in a T3SS-dependent manner, induces an early proinflammatory

20 EPEC infection inhibits RNase L in a T3SS-dependent manner, providing a mechanism by which EP

21 etion of the cytokine interleukin 1beta in a T3SS-dependent manner.

22 ork, we tested the hypothesis that SrgE is a T3SS effector by two methods, a beta-lactamase activity

23 flicting predictions as to whether SrgE is a T3SS substrate.

24 ed, we demonstrate through optimization of a T3SS injection reporter that effector injection without

25 l system, we report the first structure of a T3SS ruler protein, revealing a "ball-and-chain" archite

26 Here we have solved the first structure of a T3SS-associated PG-lytic enzyme, EtgA from enteropathoge

27 ative compounds inhibit chlamydiae through a T3SS-independent mechanism.

28 lmonella enterica serovar Typhimurium uses a T3SS encoded by Salmonella pathogenicity island 1 (SPI1)

29 ains outcompeted WT PA103 in vivo, whereas a T3SS-ON mutant showed decreased fitness compared with WT

30 r T3SS activation, yet little is known about T3SS architecture in this state or the conformational ch

31 All P. aeruginosa T3SS promoters contain two adjacent binding sites for mo

32 racterization in two different P. aeruginosa T3SS-mediated cytotoxicity assays.

33 Using the Pseudomonas aeruginosa T3SS as a model system, we report the first structure of

34 in that is structurally conserved across all T3SS-possessing pathogens, suggesting potential therapeu

35 a non-genetic origin, and the T3SS(HIGH) and T3SS(LOW) subpopulations show differences in virulence.

36 rs target host innate immune mechanisms, and T3SS-defective mutants are cleared more efficiently than

37 In vitro growth rates of WT and T3SS-OFF bacteria were determined under T3SS-inducing co

38 gs reveal the first structure of a bacterial T3SS from a major human pathogen engaged with a eukaryot

39 pD and PrgI are conserved in other bacterial T3SSs; thus, our results have wider implication in under

40 our results demonstrate that the Bordetella T3SS is required for maximal persistence and disease sev

41 Cheating by T3SS-OFF bacteria occurred only when T3SS-positive bacte

42 membrane through a translocon pore formed by T3SS proteins.

43 rovide insight into chaperone recognition by T3SS ATPases and demonstrate the importance of the chape

44 en limited work characterizing the chaperone-T3SS ATPase interaction despite it being a fundamental a

45 demonstrate the importance of the chaperone-T3SS ATPase interaction for the pathogenesis of Salmonel

46 n and ATP hydrolysis are needed for complete T3SS apparatus formation, a proper translocator secretio

47 sglycosylase families to which the conserved T3SS enzymes had been presumed to belong.

48 osa plus isogenic T3SS-OFF or constitutively T3SS-ON mutants.

49 ond to environmental changes by coordinating T3SS expression and many other biological processes.

50 ein and Naip2 is uniquely required to detect T3SS inner rod protein, but neither Naip1 nor Naip2 is r

51 te that Naip1 is uniquely required to detect T3SS needle protein and Naip2 is uniquely required to de

52 homologous components among these divergent T3SS subtypes sharing a common cytoplasmic milieu.

53 ce that the proton motive force (pmf) drives T3SS secretion in Pseudomonas aeruginosa, and that the c

54 To investigate IpaB's role during T3SS activation, we isolated secretion-deregulated IpaB

55 ound that vimentin is required for efficient T3SS translocation of effectors by S. flexneri and other

56 nd over 200 BtrA-repressed genes that encode T3SS apparatus components, secretion substrates, the Bte

57 The EPEC T3SS effector NleD counteracts this protective activity

58 for C-ring assembly by NF-T3SS and flagellar-T3SS.

59 Contact with host membranes is critical for T3SS activation, yet little is known about T3SS architec

60 ance of ubiquitous surface modifications for T3SS function, potentially explaining the broad tropism

61 s transient increase in fitness observed for T3SS-negative strains in mice contributes to the observe

62 ntial role in clearing the peptidoglycan for T3SS assembly.

63 e illuminated bacterial factors required for T3SS function, but the required host processes remain la

64 sing to an N-terminal secretion sequence for T3SS-dependent injection, three transcriptional factors,

65 utionary and functional conservation of four T3SS proteins from the Inv/Mxi-Spa family: a cytosolic c

66 sa strain CHA expressing or not a functional T3SS.

67 P. aeruginosa strain expressing a functional T3SS.

68 d with their cognate chaperones to hexameric T3SS ATPase at the bacterial membrane's cytosolic face.

69 mising therapeutic target for many important T3SS-containing pathogens.

70 One important T3SS feature is an extracellular needle with an associat

71 etermines subspecies-specific differences in T3SS expression among Bordetella species and that B. per

72 le in determining fundamental differences in T3SS phenotypes among Bordetella species.

73 The many proteins involved in T3SS construction are tightly regulated due to its role

74 ncredible post-transcriptional robustness in T3SS assembly and aids its control as a tool in biotechn

75 entify plant-derived metabolites that induce T3SS genes in Pseudomonas syringae pv tomato DC3000 and

76 wing EPEC O127:H6 strain E2348/69 infection, T3SS-dependent AE lesions and pedestals were demonstrate

77 of a virulent swine isolate and an isogenic T3SS mutant to colonize, cause disease, and be transmitt

78 T3SS-positive WT P. aeruginosa plus isogenic T3SS-OFF or constitutively T3SS-ON mutants.

79 proteins of the wild-type PPD130/91 and its T3SS ATPase DeltaesaN mutant, we identified a new effect

80 signals derived from plants to initiate its T3SS and that the level of these host-derived signals im

81 We conclude that C. rodentium uses its T3SS to induce histopathological lesions that generate a

82 witch in the regulation of early versus late T3SS substrates.

83 and the locus of enterocyte effacement (LEE) T3SSs.

84 homogeneous environment of nutrient-limited T3SS-inducing medium, suggesting that subpopulation form

85 econd regulator (Pcr1) on the inner membrane T3SS component PcrD to prevent effectors from accessing

86 t is required for the production of multiple T3SS proteins.

87 e for the closely related non-flagellar (NF) T3SS has not been observed in situ.

88 se a unified model for C-ring assembly by NF-T3SS and flagellar-T3SS.

89 that the spa33 gene encoding the putative NF-T3SS C-ring component in Shigella flexneri is alternativ

90 el for their higher order assembly within NF-T3SS.

91 Nonetheless, T3SS-negative isolates are recovered from many patients

92 Consistent with these observations, T3SS effector expression and delivery by DC3000 was impa

93 retion activity by modulating the ability of T3SS to convert pmf.

94 Sequence analysis of T3SS and flagellar ruler proteins shows that this mechan

95 ion despite it being a fundamental aspect of T3SS function.

96 ndation for the subtype-specific assembly of T3SS sorting platforms and will support further mechanis

97 Combination of T3SS-mediated GMT delivery and Activin A treatment showe

98 We report here the development of T3SS-dependent intestinal thrombotic microangiopathy (iT

99 Expression of T3SS and other virulence genes was reduced in ppGpp(0) m

100 uced amylovoran production and expression of T3SS genes.

101 The activity of EspL defines a family of T3SS cysteine protease effectors found in a range of bac

102 Increased fitness of T3SS-OFF bacteria was no longer observed at high ratios

103 e, we provide evidence that the injection of T3SS effectors does not necessarily result in cell invas

104 Mice were infected with mixtures of T3SS-positive WT P. aeruginosa plus isogenic T3SS-OFF or

105 e contributes to the observed persistence of T3SS-negative isolates in humans is of ongoing interest.

106 I secretion system (T3SS); the production of T3SS cytotoxins, and particularly ExoU, has been well es

107 sis is capable of expressing a full range of T3SS-dependent phenotypes in the presence of appropriate

108 ria was no longer observed at high ratios of T3SS-OFF to WT, a feature characteristic of bacterial ch

109 romoter, suggesting the direct regulation of T3SS cascade genes by RhpR.

110 asion are associated with down-regulation of T3SS-1 genes and class II and III (but not I) of the fla

111 n SCID mice and used it to study the role of T3SS in the pathogenesis of the disease.

112 d providing a more complete understanding of T3SS ATPase-mediated pathogen virulence.

113 vances, particularly the in situ analysis of T3SSs in contact with host membranes during chlamydial e

114 An important component of T3SSs is a conserved ATPase that captures chaperone-effe

115 A central component of T3SSs is the needle complex, a supramolecular structure

116 The central role of T3SSs in pathogenesis makes them great targets for novel

117 CsrA and neutralizes its positive effect on T3SS gene expression, flagellar formation and amylovoran

118 hermore, the requirement of ExsB for optimal T3SS assembly and activity is demonstrated using eukaryo

119 ed in this study are also relevant for other T3SS-containing Gram-negative bacteria.

120 onist and exerts tight negative control over T3SS genes.

121 cytotoxicity of two Vibrio parahaemolyticus T3SSs (T3SS1 and T3SS2) to identify human genome disrupt

122 x with the building block of the polymerized T3SS inner rod component, EscI, and that this interactio

123 xpression of an invasin (Rck) and a putative T3SS effector (SrgE).

124 nant factor for FlhDC to positively regulate T3SS expression.

125 tion of bioactive metabolites fully restored T3SS effector delivery and suppressed the enhanced resis

126 PAMP-triggered immunity (PTI) also restricts T3SS effector delivery and enhances resistance by unknow

127 y, deletion of btrA in B. pertussis revealed T3SS-mediated, BteA-dependent cytotoxicity, which had pr

128 colonic crypt hyperplasia, the C. rodentium T3SS induced an excessive expansion of undifferentiated

129 that are normally nonphagocytic and a second T3SS encoded by SPI2 to survive within macrophages.

130 increased expression of type III secretion (T3SS) genes in vitro.

131 lementing the multitude of included Shigella T3SS phenotype assays and providing a more complete unde

132 The Shigella T3SS consists of a hollow needle, made of MxiH and protr

133 e exposed needle tip complex of the Shigella T3SS, invasion plasmid antigen D (IpaD) and IpaB, have b

134 functional interchangeability of Inv/Mxi-Spa T3SS proteins acting directly at the host-pathogen inter

135 phi A occurs in a type III secretion system (T3SS) 1-independent manner and results in restrained dis

136 on, including a type three secretion system (T3SS) and effectors, are carried within a chromosomal pa

137 components of the type III secretion system (T3SS) and flagellar apparatus.

138 he antiphagocytic type III secretion system (T3SS) and induces functions counteracting neutrophil-ind

139 pression of the Type Three Secretion System (T3SS) and overexpression of non-functional flagella.

140 The type 3 secretion system (T3SS) and the bacterial flagellum are related pathogenic

141 i (EPEC) uses the type III secretion system (T3SS) effector EspL to degrade the RHIM-containing prote

142 nstrated that the type III secretion system (T3SS) effector protein ExoT plays a pivotal role in faci

143 island-1 (SPI-1) type III secretion system (T3SS) effectors and translocases to inhibit bacterial in

144 depending on the type III secretion system (T3SS) effectors encoded.

145 ExsA activates type III secretion system (T3SS) gene expression in Pseudomonas aeruginosa and is a

146 the expression of type III secretion system (T3SS) genes and bacterial virulence.

147 rulence-promoting type III secretion system (T3SS) in phytopathogenic bacteria are induced at the sta

148 ecreted through a type III secretion system (T3SS) in vitro and in vivo.

149 as inhibitors of type III secretion system (T3SS) in Yersinia spp., have an inhibitory effect on chl

150 The Yop-Ysc type III secretion system (T3SS) is a critical virulence component for the pathogen

151 The Type Three Secretion System (T3SS) is a well-studied and attractive AV target, given

152 The type III secretion system (T3SS) is essential in the pathogenesis of Yersinia pesti

153 f the E. ictaluri type III secretion system (T3SS) is upregulated by acidic pH.

154 inosa expresses a type III secretion system (T3SS) needle complex that induces NLRC4 (NOD-like recept

155 The type III secretion system (T3SS) of E. tarda has been identified as a key virulence

156 The SPI-2 type III secretion system (T3SS) of intracellular Salmonella enterica translocates

157 targeting by the type III secretion system (T3SS) of pathogenic Yersinia.

158 xB and the master type III secretion system (T3SS) regulator ExsA.

159 uginosa expresses a type 3 secretion system (T3SS) strongly associated with bacterial virulence in mu

160 sense flagellin or type 3 secretion system (T3SS) structural proteins.

161 ence factors is a type III secretion system (T3SS) that injects toxins directly into the host cell cy

162 bacteria use the type III secretion system (T3SS) to deliver effector proteins into eukaryotic host

163 yotes and use the type III secretion system (T3SS) to deliver effector proteins into host cells.

164 rodentium uses a type III secretion system (T3SS) to induce colonic crypt hyperplasia in mice, there

165 rely on a complex type III secretion system (T3SS) to inject effector proteins into host cells, take

166 ny bacteria use a type III secretion system (T3SS) to inject effector proteins into host cells.

167 s use a conserved type III secretion system (T3SS) to inject virulence effector proteins directly int

168 es a syringe-like type III secretion system (T3SS) to inject virulence or "effector" proteins into th

169 bacteria use the type III secretion system (T3SS) to inject virulence proteins into human cells to i

170 ic E. coli employ a type 3 secretion system (T3SS) to manipulate the host inflammatory response durin

171 ogen utilizes the type III secretion system (T3SS) to suppress host defense responses, and secretes p

172 EHEC employs a type III secretion system (T3SS) to translocate 50 effector proteins that hijack an

173 acteria utilize a type III secretion system (T3SS) to translocate virulence proteins into host cells

174 The Yersinia type III secretion system (T3SS) translocates Yop effector proteins into host cells

175 components of the type III secretion system (T3SS) translocon.

176 B. bronchiseptica type III secretion system (T3SS) would be required for maximal disease severity and

177 ication require a type III secretion system (T3SS), a widely conserved nanomachine responsible for th

178 the P. aeruginosa type III secretion system (T3SS), and its oligomeric nature allows for multiple com

179 s mediated by a type three secretion system (T3SS), causing the hallmark attaching and effacing (AE)

180 f the P. syringae type III secretion system (T3SS), essential for colonization of the host apoplast a

181 proteins using a type III secretion system (T3SS), which functions as a needle-like molecular machin

182 loped a bacterial type III secretion system (T3SS)-based protein delivery tool and shown its applicat

183 node involving a type III secretion system (T3SS)-exported protein, BtrA, and demonstrate its role i

184 pathogens is the type III secretion system (T3SS)-mediated delivery of effector proteins into host c

185 is occurs through type III secretion system (T3SS)-mediated injection of effectors into intestinal ep

186 of the S. flexneri type 3 secretion system (T3SS).

187 dependent upon a type III secretion system (T3SS).

188 omonas aeruginosa type III secretion system (T3SS).

189 l cytoplasm via a type III secretion system (T3SS).

190 alian cells via a type III secretion system (T3SS).

191 st cytosol with a type III secretion system (T3SS).

192 y machines is the type III secretion system (T3SS).

193 eterminant is the type III secretion system (T3SS); the production of T3SS cytotoxins, and particular

194 Type III Secretion Systems (T3SS) are complex bacterial structures that provide gram

195 Flagellar type III secretion systems (T3SS) contain an essential cytoplasmic-ring (C-ring) lar

196 All type III secretion systems (T3SS) harbor a member of the YscU/FlhB family of protein

197 gative bacteria, type III secretion systems (T3SS) occur in two evolutionarily related forms: injecti

198 use syringe-like type III secretion systems (T3SS) to inject effector proteins directly into targeted

199 em (T2SS), three type III secretion systems (T3SS), and six type VI secretion systems (T6SS).

200 1B employs two type three secretion systems (T3SS), Ysa and Ysc, which inject effector proteins into

201 Type III secretion systems (T3SSs) are complex nanomachines that export proteins fro

202 Type III secretion systems (T3SSs) are essential devices in the virulence of many Gr

203 Type III Secretion Systems (T3SSs) are structurally conserved nanomachines that span

204 e depends on two type III secretion systems (T3SSs) encoded in two distinct Salmonella pathogenicity

205 al pathogens use type III secretion systems (T3SSs) for virulence.

206 Type III secretion systems (T3SSs) inject bacterial effector proteins into host cell

207 Type 3 secretion systems (T3SSs) of bacterial pathogens translocate bacterial effe

208 athogens utilize type III secretion systems (T3SSs) to inject bacterial effector proteins into the ho

209 species utilize type III secretion systems (T3SSs) to translocate effectors into the cytosol of mamm

210 ins of bacterial type III secretion systems (T3SSs).

211 o host cells via type III secretion systems (T3SSs).

212 detailed regulatory networks of QS systems, T3SS, and antibiotic resistance.

213 ve mutants are cleared more efficiently than T3SS-positive bacteria by an immunocompetent host.

214 imurium T3SS inner rod protein PrgJ and that T3SS inner rod proteins from multiple bacterial species

215 Our findings indicate that T3SS-negative isolates benefit from the public good prov

216 The T3SS translocator proteins YopB and YopD form pores in h

217 PcrD to prevent effectors from accessing the T3SS, and (ii) In conjunction with PscO, it controls pro

218 Through NLRC4 inflammasome activation, the T3SS promotes IL-18 secretion, which dampens a beneficia

219 at human NAIP detects both flagellin and the T3SS needle protein and suggested that the ability to de

220 ic target cell has been established, and the T3SS proteins YscP and YscU play a central role in this

221 Both the urease and the T3SS were previously shown to be essential to intracellu

222 le, indicating a non-genetic origin, and the T3SS(HIGH) and T3SS(LOW) subpopulations show differences

223 d the primary target of the compounds as the T3SS needle pore protein EspD, which is essential for ef

224 To assemble, the T3SS must traverse both bacterial membranes, as well as

225 ein tightly regulates the length of both the T3SS and the flagellum, but the molecular basis for this

226 rsinia-specific sRNA, Ysr141, carried by the T3SS plasmid pCD1 that is required for the production of

227 pseudotuberculosis YscU, is secreted by the T3SS when bacteria are grown in Ca(2+)-depleted medium a

228 tially by detecting FliC translocated by the T3SS, whereas the bacteria downregulate the expression o

229 nt vimentin as required for infection by the T3SS-dependent pathogen S. flexneri.

230 he aim of this study was to characterize the T3SS effector EspW.

231 'tip complex' translocator that connects the T3SS needle to the translocon pore.

232 cs and regulatory mechanisms controlling the T3SS and pathogen virulence remain largely unclear.

233 of the entire chromosomal locus encoding the T3SS, further demonstrating their desirability and effec

234 However, the T3SS mutant and the wild-type parent are equally capable

235 ing P. aeruginosa, which is deficient in the T3SS needle complex, did not alter the excessive IL-1bet

236 gene operon suggested an implication in the T3SS regulation, while its similarity with yscW from Yer

237 an sRNA that influences the synthesis of the T3SS adds an additional layer of regulation to this tigh

238 idify would prevent both upregulation of the T3SS and activation of the urease enzyme, either of whic

239 block in the synthesis of a component of the T3SS apparatus and an effector.

240 We report a new role of the T3SS apparatus itself, independently of exotoxin translo

241 rG interacts with distinct components of the T3SS apparatus to control two important aspects of effec

242 tor, to couple the secretory activity of the T3SS apparatus to gene expression.

243 , thereby preventing correct assembly of the T3SS complex on the cell surface.

244 The structural component of the T3SS contains a needle and a needle tip.

245 EC and shed light on the complexities of the T3SS effector repertoires of Enterobacteriaceae.

246 P. aeruginosa infection as a function of the T3SS effectors produced by the infecting strain.

247 n Hfq in the regulation of components of the T3SS in the gastrointestinal pathogen Yersinia pseudotub

248 ntribution of sRNAs to the regulation of the T3SS in Yersinia has been largely unstudied, however.

249 ntial passage through the inner lumen of the T3SS needle.

250 ompounds that block the functionality of the T3SS of EHEC.

251 to be essential for the up-regulation of the T3SS on host cell contact.

252 op involving HrpA, the main component of the T3SS pilus.

253 Inadvertent injection of the T3SS rod protein and flagellin into the cytosol is detec

254 articular, ExsB promotes the assembly of the T3SS secretin in the bacterial outer membrane, highlight

255 n and post-transcriptional regulation of the T3SS through Hfq.

256 To examine the contribution of the T3SS to the pathogenesis of B. bronchiseptica in swine,

257 ) were used to study the contribution of the T3SS transcriptional activator ExsA to epithelial traver

258 centration, which triggers activation of the T3SS, directly influences the cytosolic complexes, possi

259 ute to its function in the regulation of the T3SS.

260 the protrusion membrane, which relies on the T3SS-dependent activation of tyrosine kinase signaling i

261 tion and translocation of EseJ depend on the T3SS.

262 the corresponding feedback inhibition on the T3SS.

263 he T3SS needle protein, NAIP2 recognizes the T3SS inner rod protein, and NAIP5 and NAIP6 recognize fl

264 NAIP1 recognizes the T3SS needle protein, NAIP2 recognizes the T3SS inner rod

265 and compared their abilities to regulate the T3SS and influence host cell survival in vitro.

266 romote enterocyte survival by regulating the T3SS and/or by modulating epithelial signaling pathways.

267 human NAIP isoform is capable of sensing the T3SS inner rod, needle, and flagellin.

268 ion will need to extend beyond targeting the T3SS.

269 of Bacteriology, Roblin et al. show that the T3SS chaperone SigE of Salmonella can form hexameric rin

270 nce gene products were produced and that the T3SS effector EspB of EPEC, and heat-labile toxin of ETE

271 icrobe, Guo et al. (2016) determine that the T3SS effector, HopE1, targets calmodulin and the microtu

272 We found that the T3SS is required for maximal persistence throughout the

273 e mechanism for how bacteria ensure that the T3SS needles are neither too short nor too long.

274 In this study, we report that the T3SS of E. tarda facilitates its survival and replicatio

275 Our data further suggest that the T3SS skews the adaptive immune response in swine by hind

276 In conclusion, EPEC, through the T3SS-dependent translocation of NleF, induces a proinfla

277 nt in blocking protein secretion through the T3SS.

278 in regulating protein secretion through the T3SS.

279 ray analysis showed that, in addition to the T3SS cascade genes, RhpR differentially regulates a larg

280 latory mechanisms that link the FlhDC to the T3SS through three distinct pathways including the FlhDC

281 s strain delivering the LcrV antigen via the T3SS as a potential vaccine candidate against pneumonic

282 and invade colonic epithelial cells via the T3SS.

283 While the T3SS is known to be involved in disease in vivo, how it

284 How these regulators interface with the T3SS apparatus to control secretion is unclear.

285 inus of the ruler protein interacts with the T3SS autoprotease in the cytosolic side.

286 pD(Delta207-227) mutants and analyzing their T3SS functions.

287 he associated effectors translocated by this T3SS.

288 association resulted in decreased binding to T3SS promoters, particularly loss of binding by the seco

289 genome disruptions conferring resistance to T3SS-dependent cytotoxicity.

290 ture of the primordial Chlamydia trachomatis T3SS in the presence and absence of host membrane contac

291 of food-borne gastroenteritis, possesses two T3SSs, one belonging to the Inv/Mxi-Spa family.

292 veal a novel strategy in which S Typhimurium T3SS effectors broaden their functions through the activ

293 NAIP also senses the Salmonella Typhimurium T3SS inner rod protein PrgJ and that T3SS inner rod prot

294 and T3SS-OFF bacteria were determined under T3SS-inducing conditions and did not differ significantl

295 ngth sensing by ruler proteins, whereby upon T3SS needle assembly, the ruler protein's N-terminal end

296 by S. flexneri and other pathogens that use T3SS, Salmonella enterica serovar Typhimurium and Yersin

297 ting by T3SS-OFF bacteria occurred only when T3SS-positive bacteria expressed the phospholipase A2 ef

298 inosa infections, leading us to test whether T3SS-negative strains could have a selective advantage d

299 , Chung et al. (2016) show that the Yersinia T3SS effector protein YopM counteracts this recognition

300 litica mutants lacking either the Ysa or Ysc T3SS were partially defective, while double mutants were