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1 T6SS activity is silenced in plasmid-containing, antibio
2 T6SS and plasmid conjugation both involve cell-to-cell c
3 T6SS is regulated at transcriptional and posttranslation
4 T6SS sheaths are cytoplasmic tubular structures composed
5 T6SSs are a class of sophisticated cell contact-dependen
7 at one of these, type VI secretion system 5 (T6SS-5), is required for virulence in mammalian infectio
8 ism by bacterial type VI secretion system 5 (T6SS-5), which is an essential virulence factor in both
10 n 11 167 core T6SS components mapping to 906 T6SSs found in 498 bacterial strains representing 240 sp
12 6, an anti-bacterial effector delivered by a T6SS of the opportunistic pathogen Serratia marcescens,
15 also show the TleV1 toxin is delivered in a T6SS manner by V. cholerae and can lyse other bacterial
24 ella enterica serovar Typhimurium requires a T6SS encoded within Salmonella pathogenicity island-6 (S
26 P. aeruginosa adapts to the CF lung abrogate T6SS activity, making P. aeruginosa and its human host s
32 rrays of immunity genes that protect against T6SS-mediated intra- and inter-species bacterial antagon
34 chanism that modulates the deployment of all T6SS weapons that may be simultaneously produced within
37 of global control by RsmA to VgrG spike and T6SS toxin transcripts whose genes are scattered on the
39 effector-immunity paradigm for antibacterial T6SS substrates, the toxic activities of these effectors
40 ate that several MIX-containing proteins are T6SS effectors and that they are not required for T6SS a
42 cterial virulence protein expression because T6SS-1 and some effectors of type 3 secretion system 3 (
44 with single-cell analysis of combat between T6SS-wielding Acinetobacter baylyi and T6SS-sensitive Es
46 del whereby the CTD of VgrG-5-, propelled by T6SS-5-, plays a key role in inducing membrane fusion, e
47 ly shown and/or predicted to be delivered by T6SSs into target eukaryotic and/or prokaryotic cells as
49 is result also demonstrated that V. cholerae T6SS is capable of delivering effectors that could attac
50 It currently contains data on 11 167 core T6SS components mapping to 906 T6SSs found in 498 bacter
53 seudomonas aeruginosa encodes three distinct T6SS haemolysin coregulated protein (Hcp) secretion isla
54 confirmed that these differences distinguish T6SS classes that resulted from a functional co-evolutio
55 approach, we discovered that the FPI-encoded T6SS exports at least three effectors encoded outside of
56 proach to the Hcp secretion island I-encoded T6SS (H1-T6SS) of Pseudomonas aeruginosa led to the iden
58 . pseudomallei strains engineered to express T6SS-5 in vitro show that the VgrG5 C-terminal domain is
60 croscopy reveals that they assemble and fire T6SS contractile sheaths at ~6% of the frequency of rhs
62 a coli target bacteria and are defective for T6SS-dependent export of hemolysin-coregulated protein (
63 e VgrG5 C-terminal domain is dispensable for T6SS-mediated secretion of Hcp5, demonstrating that the
67 , Rhs proteins are not strictly required for T6SS assembly, although they greatly increase secretion
68 al adherence, and we identify a new role for T6SS as a key virulence factor in gastrointestinal infec
69 kely represents an evolutionary strategy for T6SS effectors to reach their intended substrates regard
71 d that B. pseudomallei requires a functional T6SS for full virulence, bacterial dissemination, and le
72 d to Bacteroides fragilis Unlike GA1 and GA2 T6SS loci, most GA3 loci do not encode identifiable effe
74 ned in two variable regions of GA3 loci, GA3 T6SSs of the species B. fragilis are likely the source o
79 r screen failed to identify two predicted H1-T6SS effectors, Tse5 and Tse6, which differ from Hcp-sta
81 the Hcp secretion island I-encoded T6SS (H1-T6SS) of Pseudomonas aeruginosa led to the identificatio
83 the independent contribution of the three H1-T6SS co-regulated vgrG genes, vgrG1abc, to bacterial kil
84 th respect to the requirement for the two H1-T6SS-exported VgrG proteins, whereas Tse5 and Tse6 deliv
85 Here we performed a screen to identify H2-T6SS and H3-T6SS regulatory elements and found that the
86 at the type VI secretion system locus II (H2-T6SS) of P. aeruginosa delivers AmpDh3 (but not AmpD or
88 ggered the characterization of a suite of H2-T6SS toxins and their implication in direct bacterial co
90 an evolutionary advantage and that of the H2-T6SS as the means for the manifestation of the effect.
91 e the characterization of a P. aeruginosa H3-T6SS-dependent phospholipase D effector, PldB, and its t
93 erformed a screen to identify H2-T6SS and H3-T6SS regulatory elements and found that the posttranscri
94 tein (Hcp) secretion islands (H1, H2, and H3-T6SS), each involved in different aspects of the bacteri
95 e renamed TseF) appears to be secreted by H3-T6SS and is incorporated into outer membrane vesicles (O
96 ximal to the type VI secretion system H3 (H3-T6SS), functions synergistically with known iron acquisi
97 of susceptible P. aeruginosa isolates harbor T6SS-abrogating mutations, the repair of which, in some
100 SS effector (TseL) of V. cholerae can induce T6SS dynamic activity in P. aeruginosa when delivered to
102 eudomonas aeruginosa assembles and fires its T6SS apparatus only after detecting initial attacks by o
103 is a Gram-negative pathogen that can use its T6SS during antagonistic interactions with neighboring p
105 yse its parental strain upon contact via its T6SS but is unable to kill parental cells expressing the
107 dicted to transit not only the Gram-negative T6SS but also the Gram-positive type VII secretion syste
114 er, the identification and mode of action of T6SS effector proteins that mediate this protective effe
116 as polymyxin B can also trigger assembly of T6SS organelles via a signal transduction pathway that i
118 dy of the evolutionary costs and benefits of T6SS weaponry during competition with other bacteria.
123 likely responsible for the high diversity of T6SS effector-immunity gene profiles observed for V. cho
127 cid pH upregulates the expression of Hcp1 of T6SS-1 and TssM, a protein coregulated with T6SS-1.
129 ta, which suggest that the great majority of T6SS-wielding species do indeed use lytic toxins, indica
130 bacterial fitness, systematic prediction of T6SS effectors remains challenging due to high effector
131 ly, these analyses uncover the prevalence of T6SS-dependent competition and reveal its potential role
134 dies suggest that the complete repertoire of T6SS effectors delivered to host cells is encoded by the
138 ion substrates of the T6SS and one subset of T6SS effectors consists of VgrG proteins with C-terminal
139 cations that describe three superfamilies of T6SS proteins, each dedicated to mediate the secretion o
145 Our findings provide an example of pathogen T6SS-dependent killing of commensal bacteria as a mechan
146 Recent work suggests that a phospholipase T6SS effector (TseL) of V. cholerae can induce T6SS dyna
147 Phylogenetic analysis of phytobacterial T6SS clusters shows that they are distributed in the fiv
150 tructure of a sheath protein complex propels T6SS spike and tube components along with antibacterial
156 as the Bptm group, appear to encode several T6SSs, we and others have shown that one of these, type
159 we report that the type 6 secretion system (T6SS) and type 1 fimbriae are important virulence factor
175 The bacterial type VI secretion system (T6SS) is a supra-molecular complex akin to bacteriophage
179 he P. chlororaphis type VI secretion system (T6SS) is activated upon contact with B. subtilis cells,
180 The bacterial type VI secretion system (T6SS) is an organelle that is structurally and mechanist
183 ecently discovered type VI secretion system (T6SS) is widespread in bacterial pathogens and used to d
184 The bacterial type VI secretion system (T6SS) mediates antagonistic cell-cell interactions betwe
185 nactivation of the type VI secretion system (T6SS) of a competitor annuls the responses to competitio
186 ompetitors via the Type VI secretion system (T6SS) precipitates phase separation via the 'Model A' un
188 contact-dependent type VI secretion system (T6SS) that kills neighbouring competitors by translocati
189 bour genes for the type VI secretion system (T6SS) that translocates effectors into neighbouring euka
190 cholerae use their type VI secretion system (T6SS) to actively acquire DNA from non-kin neighbors.
191 oys a harpoon-like type VI secretion system (T6SS) to compete against other microbes in environmental
194 ocepacia employs a type VI secretion system (T6SS) to survive in macrophages by disarming Rho-type GT
196 onism, such as the type VI secretion system (T6SS), a multiprotein needle-like apparatus that injects
197 aumannii encodes a type VI secretion system (T6SS), an antibacterial apparatus of Gram-negative bacte
198 res (GA1-3) of the type VI secretion system (T6SS), an effector delivery pathway that mediates interb
199 nregulation of the type VI secretion system (T6SS), and prevents T6SS-dependent bacterial killing by
200 n system (T2SS), a type VI secretion system (T6SS), autotransporter, and outer membrane vesicles (OMV
201 d component of the type VI secretion system (T6SS), haemolysin co-regulated protein (Hcp), binds dire
202 onism, such as the type VI secretion system (T6SS), have not been defined in this group of organisms.
204 oidales encode the type VI secretion system (T6SS), which facilitates the delivery of toxic effector
206 tive cells against type VI secretion system (T6SS)-wielding competitors, including physical barriers,
211 n of the cluster 5 type VI secretion system (T6SS-5) and its associated valine-glycine repeat protein
214 been described: type six secretion systems (T6SS); contact dependent inhibition (CDI); and bacterioc
218 d proteobacteria, type VI secretion systems (T6SSs) are potentially capable of facilitating diverse i
221 how that unlike the bacterial-cell-targeting T6SSs characterized so far, T6SS-5 localizes to the bact
224 he responses to competition, indicating that T6SS-derived cell damage activates these stress response
231 n be sensed by P. aeruginosa to activate the T6SS even when the disruption is generated by aberrant c
232 portance of the extracellular matrix and the T6SS in modulating the coexistence of the two species on
237 Finally, we discuss the roles played by the T6SS of V. cholerae in both natural environments and hos
239 work illustrates the twin role played by the T6SS, dealing death to local competitors while simultane
241 to directly targeting eukaryotic cells, the T6SS can also target other bacteria coinfecting a mammal
242 d to other bacteria, c-di-GMP turns down the T6SS in A. tumefaciens thus impacting its ability to com
245 indings to our developing picture of how the T6SS assembles and fires, how it is loaded with differen
248 e core conserved secretion substrates of the T6SS and one subset of T6SS effectors consists of VgrG p
250 regarding the structure and function of the T6SS as well as the diverse signals and regulatory pathw
251 TssA1 could be a baseplate component of the T6SS Furthermore, we identified similarities between Tss
253 ws the phylogeny and biological roles of the T6SS in plant-associated bacteria, highlighting a remark
254 idespread occurrence and significance of the T6SS is becoming increasingly appreciated, as is its int
258 , that, interestingly, are homologues of the T6SS membrane complex components TssL and TssM, suggesti
259 ian host, highlighting the importance of the T6SS not only for bacterial survival in environmental ec
260 Our results indicate a new model of the T6SS organelle in which the VgrG-PAAR spike complex is d
267 that multivalent nanoparticles based on the T6SS sheath represent a versatile scaffold for vaccine a
268 on their distinctive ability to repress the T6SS of their hosts to enable their own dissemination an
269 ural biology and live-cell imaging shows the T6SS as a long contractile sheath assembled around a rig
272 gut in an Hcp1-dependent manner and that the T6SS antibacterial activity is essential for Salmonella
273 d pathogenic phytobacteria suggests that the T6SS provides fitness and colonization advantages in pla
274 nchial epithelial cells, indicating that the T6SS-5 is important in the host-pathogen interaction in
276 fatal water-borne cholera disease, uses the T6SS to evade phagocytic eukaryotes, cause intestinal in
279 species, such as Vibrio cholerae, use their T6SS in an untargeted fashion while in contrast, Pseudom
280 a of the order Bacteroidales, and that these T6SS loci segregate into three distinct genetic architec
281 experimentally confirm the identity of this T6SS and, by cryo electron microscopy (cryoEM), show the
284 ve pathogen Pseudomonas aeruginosa has three T6SSs involved in colonization, competition, and full vi
285 d the conditions of the DNA released through T6SS-mediated killing versus passive cell lysis and the
287 h induced soxS in E. coli expressing a toxic T6SS antibacterial effector and in E. coli treated with
288 review, we highlight the repertoire of toxic T6SS effectors and the diverse genetic regulation networ
289 n outer membrane biogenesis can also trigger T6SS activation in P. aeruginosa Specifically, we develo
292 ore, we provide evidence that one of the two T6SS nanotube subunits, Hcp1, is required for killing Kl
293 e identification of numerous uncharacterized T6SS effectors that will undoubtedly lead to the discove
298 Our findings imply a potentially widespread T6SS-mediated mechanism, which deploys a single phosphol