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 effector intoxication was sufficient to generate cy

5 T3SS effectors are thought to be inactive within the bac

6 T3SS expression is bistable in the homogeneous environme

7 T3SS-dependent invasion of epithelial cells is necessary

8 T3SSs involved in virulence (vT3SSs) are evolutionarily

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

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

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

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

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

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

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

16 The N terminus of mature TDH comprises a T3SS signal sequence, allowing it to be loaded into the

17 ge, the first intra-bacterial activity for a T3SS effector and show that arginine-GlcNAcylation, once

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 estis also inhibits release of granules in a T3SS-dependent manner.

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

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

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

25 od-borne diarrheal disease, we showed that a T3SS effector, VgpA, localizes to the host cell nucleolu

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

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

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

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

30 n to identify metabolic pathways that affect T3SS expression.

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

32 n factor ExsA activates transcription of all T3SS-associated genes.

33 with transcriptional activation of axoU and T3SS genes, demonstrating that this model can be used as

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

35 ty island, including the adhesin Intimin and T3SS filament EspA, which are major antigens conferring

36 However, blocking both Psl and T3SS together with antibiotic treatment broke down the b

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 pabilities in detecting pathogenic bacterial T3SS-associated antigens as well as intact bacteria.

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 but in addition a second T3SS termed E. coli T3SS 2 (ETT2) has been described in a number of strains

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

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

46 Conversely, T3SS-incompetent P aeruginosa infection produced non-cyt

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

48 agic Escherichia coli contain a well-defined T3SS but in addition a second T3SS termed E. coli T3SS 2

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

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

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

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

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

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

55 The EPEC T3SS effector NleD counteracts this protective activity

56 A fourth essential T3SS protein (FlhB/SctU) functions to "switch" secretion

57 action of PscN with a wide range of exported T3SS proteins including the needle, translocator, gate-k

58 erone dissociation and unfolding of exported T3SS proteins.

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

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

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

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

63 ntial role in clearing the peptidoglycan for T3SS assembly.

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

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

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

67 P aeruginosa possessing a functional T3SS and effectors induced the production and release of

68 sa strain CHA expressing or not a functional T3SS.

69 he development of colonic crypt hyperplasia, T3SS-mediated intimate attachment is not required for ae

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

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

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

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

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

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

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

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

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

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

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

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

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

83 During infection, the syringe-like T3SS injects cytotoxic proteins directly into the eukary

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

85 Common to many T3SSs is that injection of effector proteins is feedback

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

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

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

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

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

98 uced amylovoran production and expression of T3SS genes.

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

100 ight relieve the ExsD-mediated inhibition of T3SS gene expression, because the same region of ExsD in

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

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

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

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

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

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

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

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

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

110 nderstanding of the pathogenic mechanisms of T3SSs.

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

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

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

114 fold, like that of its homologues from other T3SS.

115 onist and exerts tight negative control over T3SS genes.

116 The Vibrio parahaemolyticus T3SS effector VopQ targets host-cell V-ATPase, resulting

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

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

119 nant factor for FlhDC to positively regulate T3SS expression.

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

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

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

123 he homologous interactions in the Salmonella T3SS sorting platform revealed clear differences in thei

124 a well-defined T3SS but in addition a second T3SS termed E. coli T3SS 2 (ETT2) has been described in

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

126 nce this epitope is conserved across several T3SS-harboring pathogens, mAb-EspB-B7 holds great potent

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

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

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

130 Since T3SS secreted effectors (T3SEs) play important roles in

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

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

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

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

135 enzymes (PCWDEs), type III secretion system (T3SS) and flagellar motility.

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

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

138 secreted it via the type 3 secretion system (T3SS) at 37 degrees C under calcium-deprived conditions.

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

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

141 ichia coli (EPEC) type III secretion system (T3SS) effector translocated intimin receptor (Tir) by in

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

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

144 the importance of type III secretion system (T3SS) effectors in the production of cytotoxic amyloids.

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

146 The type III secretion system (T3SS) is a pivotal virulence mechanism of many Gram-nega

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

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

149 ement (LEE)-encoded type 3 secretion system (T3SS) is the major virulence determinant of EPEC and is

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

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

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

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

154 c bacterium whose type III secretion system (T3SS) plays a critical role in acute infections.

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

156 by the conserved type III secretion system (T3SS) rod proteins from Gram-negative bacteria or noncan

157 ow that AxoU is a type III secretion system (T3SS) substrate that induces cytotoxicity to mammalian c

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

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

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

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

162 aeruginosa uses a type III secretion system (T3SS) to inject cytotoxic effector proteins into host ce

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

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

165 e machinery named type-III secretion system (T3SS) to inject effectors within host cells that lead to

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

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

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

169 e pathogens use a type III secretion system (T3SS) to promote disease by injecting effector proteins

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

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

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

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

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

175 island 1 (SPI-1) type III secretion system (T3SS)) and outer membrane (OM) (15-mer InvG, a member of

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

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

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

179 orted through the type III secretion system (T3SS), which engages in one-step secretion of effectors(

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

181 ithin the bacterial type 3 secretion system (T3SS), which is mainly expressed in Gram-negative pathog

182 expression of the Type III secretion system (T3SS), widely considered to be the most potent virulence

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

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

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

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

187 rypt hyperplasia, type III secretion system (T3SS)-mediated intimate epithelial attachment provides C

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

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

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

191 omonas aeruginosa type III secretion system (T3SS).

192 to host cells via a type 3 secretion system (T3SS).

193 e factors through a type 3 secretion system (T3SS).

194 y island 1 (SPI1) type III secretion system (T3SS).

195 on of the bacterial type-3 secretion system (T3SS).

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

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

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

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

200 retion through type-three secretion systems (T3SS) is critical for motility and virulence of many bac

201 Pathogen type 3 secretion systems (T3SS) manipulate host cell pathways by directly deliveri

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

203 al pathogens use type III secretion systems (T3SS) to inject proteins into eukaryotic cells to subver

204 n cells by using type III secretion systems (T3SS) to inject virulence proteins into host cells.

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

206 1B employs two type three secretion systems (T3SS), Ysa and Ysc, which inject effector proteins into

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

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

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

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

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

212 ffectors through Type III secretion systems (T3SSs) into host cells and cause diseases.

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

214 Bacterial type III secretion systems (T3SSs) play an important role in pathogenesis of Gram-ne

215 ive bacteria use type III secretion systems (T3SSs) to inject virulence effector proteins into eukary

216 ll cytoplasm via type III secretion systems (T3SSs) to modulate interactions between Gram-negative ba

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

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

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

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

221 ssue of Immunity, Wu et al. (2019) show that T3SS rod proteins or LPS induces inflammasome activation

222 We also show that T3SS-delivered TDH as an effector contributes to intesti

223 The T3SS apparatus (injectisome) shares a common architectur

224 The T3SS apparatus (T3SA) is structurally conserved among di

225 The T3SS regulon genes are regulated by an AraC-type regulat

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

227 In addition, the T3SS promotes the intracellular growth of P. aeruginosa

228 PecT down-regulates PCWDE and the T3SS by repressing the expression of a global post-trans

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

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

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

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

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

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

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

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

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

238 ation of early substrates recognition by the T3SS.

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

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

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

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

243 tivates expression of the genes encoding the T3SS.

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

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

246 at a series of conformational changes in the T3SS trigger opening of the gate through interactions be

247 sequence, allowing it to be loaded into the T3SS.

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

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

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

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

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

253 Translocation of the T3SS effectors into host cells induces cytotoxicity.

254 In Pseudomonas aeruginosa, expression of the T3SS is regulated by a signaling cascade involving the p

255 his was unexpected because expression of the T3SS is usually reciprocally coordinated with T6 secreti

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

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

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

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

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

261 ption of hilA, encoding the activator of the T3SS structural genes.

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

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

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

265 tion and translocation of EseJ depend on the T3SS.

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

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

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

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

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

271 ion will need to extend beyond targeting the T3SS.

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

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

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

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

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 ous work established that Y. pestis uses the T3SS to inhibit neutrophil respiratory burst, phagocytos

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

283 port mechanism for a bacterial toxin via the T3SS in tandem with the Sec machinery facilitates the vi

284 and invade colonic epithelial cells via the T3SS.

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

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

287 hibits the functions of macrophages with the T3SS.

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

289 he associated effectors translocated by this T3SS.

290 genome disruptions conferring resistance to T3SS-dependent cytotoxicity.

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

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

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

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

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

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

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

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

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

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