ライフサイエンスコーパス: A. tumefaciens

1 that restored pathogenicity to virE2 mutant A. tumefaciens.

2 the VirD4 coupling protein at cell poles of A. tumefaciens.

3 ate complex to division sites of E. coli and A. tumefaciens.

4 E. coli and homotypic complexes of VirB10 in A. tumefaciens.

5 pH, which is similar to what is observed in A. tumefaciens.

6 ncation and insertion mutants synthesized in A. tumefaciens.

7 logy and arrangement with the virB operon of A. tumefaciens.

8 ion with sequence homology to the vir box of A. tumefaciens.

9 18 amino acids, renders it non-functional in A. tumefaciens.

10 ensing mechanism found in the virB operon of A. tumefaciens.

11 gation factor is present as a single copy in A. tumefaciens.

12 likely involving an unidentified vir gene in A. tumefaciens.

13 as found to be essential for partitioning in A. tumefaciens.

14 84, G665D) in Escherichia coli as well as in A. tumefaciens.

15 ability of TraM to inhibit wild-type TraR in A. tumefaciens.

16 in which the alpha subunit was derived from A. tumefaciens.

17 its VirE2 protein, but not T-DNA export from A. tumefaciens.

18 ng expression in the plant after delivery by A. tumefaciens.

19 ive pilus, hereafter called the "T pilus" of A. tumefaciens.

20 ly controls the expression of three sRNAs in A. tumefaciens.

21 t, which encodes isopentenyl transferase, in A. tumefaciens.

22 extension of R. meliloti FtsZ1 was found in A. tumefaciens.

23 FliP are required for flagellar assembly in A. tumefaciens.

24 nstructs were maintained in both E. coli and A. tumefaciens.

25 ssDNA) binding, and accumulation of VirE2 in A. tumefaciens.

26 a single-copy plasmid in both E. coli and in A. tumefaciens.

27 t virE2, decreased the stability of VirE2 in A. tumefaciens.

28 oli appears to differ from that predicted in A. tumefaciens.

29 ansfer, we developed an expression system in A. tumefaciens.

30 is required for synthesis of this polymer in A. tumefaciens.

31 glycophorin A blocked T-pilus biogenesis in A. tumefaciens.

32 regulate the motile to non-motile switch in A. tumefaciens.

33 B. subtilis, with no impact on attraction of A. tumefaciens.

34 nd was utilized as sole source of sulphur by A. tumefaciens.

35 idence for twitching or swarming motility in A. tumefaciens.

36 tial for As(III) oxidation in this strain of A. tumefaciens.

37 n be restored by the delivery of AvrRpt2 via A. tumefaciens.

38 lled TraM2, not encoded on the Ti plasmid of A. tumefaciens A6, was identified, in addition to a copy

39 ually nothing was previously known about how A. tumefaciens acquires sulphur during colonization.

40 The A. tumefaciens ADPGlc PPase model was refined to 2.1 A w

41 The A. tumefaciens ADPGlc PPase/fructose 6-phosphate structu

42 ains the N-terminus (271 amino acids) of the A. tumefaciens ADPglucose pyrophosphorylase and the C-te

43 A. tumefaciens also has two additional pleC/divJhomologu

44 in in numerous predicted sensing proteins in A. tumefaciens and other bacteria, indicating that AtBph

45 and related c-di-GMP-dependent phenotypes in A. tumefaciens and potentially acts more widely in multi

46 ectively transported into the plant pathogen A. tumefaciens and processed into the toxin TM84.

47 Furthermore, while the A. tumefaciens and R. meliloti donors produced high leve

48 action between VirG and the alpha subunit of A. tumefaciens and that the alpha subunit from E. coli i

49 ucleotide colinearity between the genomes of A. tumefaciens and the plant symbiont Sinorhizobium meli

50 imilarity between the processing of VirB2 in A. tumefaciens and the processing of the propilin TraA o

51 ork expands the model for ExoR regulation in A. tumefaciens and underscores the global role that this

52 re, we examine chemical interactions between A. tumefaciens and unwounded plants.

53 by tobacco and Arabidopsis when colonized by A. tumefaciens and was utilized as sole source of sulphu

54 ble regeneration capacity and amenability to A. tumefaciens and, the resulting transformants have lar

55 irE1, (iii) accumulate at abundant levels in A. tumefaciens, and (iv) restore wild-type virulence to

56 f genes via manipulation of sRNA pathways in A. tumefaciens, and moreover, while the VtlR/LsrB protei

57 o a T-DNA vector plasmid and introduced into A. tumefaciens, and the resultant strain was used for co

58 activation events in signal transduction in A. tumefaciens, and we expect it to be useful in other p

59 A. tumefaciens appears to transfer T-DNA into plant cell

60 indicate that the att (attachment) genes of A. tumefaciens are crucial in the ability of this soil p

61 ivJ-DivK and CckA-ChpT-CtrA phosphorelays in A. tumefaciens are vertically-integrated, as in C. cresc

62 ffect on attempts to transform corn by using A. tumefaciens as a vector.

63 In summary, regulation of A. tumefaciens As(III) oxidation is complex, apparently

64 s two substrates of recombinant METTL20 from A. tumefaciens (AtMETTL20), namely ETFbeta and the ribos

65 A. tumefaciens attaches efficiently to plant tissues and

66 SinR is required for normal maturation of A. tumefaciens biofilms on both inert surfaces and plant

67 ygen levels, and influences the formation of A. tumefaciens biofilms.

68 As predicted the A. tumefaciens biotin protein ligase is a fully function

69 n is further cyclized to form the T pilin in A. tumefaciens but not in E. coli.

70 provide evidence that the alpha subunit from A. tumefaciens, but not from E. coli, is able to interac

71 hese virE2 genes respond to virE2 mutants of A. tumefaciens by forming wild-type tumours.

72 nced and compared with homologous regions of A. tumefaciens C58 and Sinorhizobium meliloti Rm1021 gen

73 We isolated four Tn5-induced mutants of A. tumefaciens C58 deficient in TraR-mediated activation

74 The A. tumefaciens C58 genome sequence revealed the presence

75 A search of the genome of A. tumefaciens C58 revealed four proteins, encoded on di

76 Adherence of A. tumefaciens C58 was significantly enhanced under phos

77 The genome of a biovar I strain, A. tumefaciens C58, has been previously sequenced.

78 nctions encoded on the two large plasmids of A. tumefaciens C58, pTiC58 and pAtC58, were not required

79 ::p50 constructs are infected with oncogenic A. tumefaciens C58, transgenic lines harbouring the 2S2D

80 the previously published genome sequence of A. tumefaciens C58.

81 A. tumefaciens C58::A205 (C58 attR) is a Tn3HoHo1 insert

82 BioR sites of Brucella plus the BioR site of A. tumefaciens can all interact with the Brucella BioR p

83 We show that the host range of A. tumefaciens can be extended to include Saccharomyces

84 A. tumefaciens can transfer its T-DNA to a wide variety

85 Overexpression of RepC in A. tumefaciens caused large increases in copy number in

86 Depletion of FtsZ(AT) in A. tumefaciens causes a striking phenotype: cells are ex

87 required for T-DNA translocation across the A. tumefaciens cell envelope.

88 ti-GFP antibodies from detergent-solubilized A. tumefaciens cell extracts.

89 VirD4, and Osa-GFP colocalizes with VirD4 at A. tumefaciens cell poles.

90 expression, as determined by infection with A. tumefaciens cells carrying the beta-glucuronidase int

91 ontrolling this biphasic reaction in induced A. tumefaciens cells revealed that virA on the Ti plasmi

92 ots and reduced ability of the roots to bind A. tumefaciens cells under certain conditions.

93 kaline phosphatase activities in E. coli and A. tumefaciens cells, providing genetic evidence for the

94 tive dominance when synthesized in wild-type A. tumefaciens cells.

95 umefaciens localized to the division site in A. tumefaciens cells.

96 transformed using a short cocultivation with A. tumefaciens cells.

97 The region downstream of the A. tumefaciens chvE gene was cloned and sequenced for nu

98 revealed the existence of a newly discovered A. tumefaciens chvI homolog located just upstream of the

99 3 mM DIMBOA is sufficient to block growth of A. tumefaciens completely for 220 hr.

100 When A. tumefaciens contained osa, the lack of expression of

101 opriate stage of growth, are inoculated with A. tumefaciens containing the binary vector.

102 d TraM appear to function similarly to their A. tumefaciens counterparts, the TraR and TraM orthologu

103 G, and cysT from Escherichia coli; occP from A. tumefaciens; cysA from Synechococcus spp.; and ORF-C

104 served orthologues appear to be essential in A. tumefaciens, deletions in pleC or divK were isolated

105 nonmotile, or flagellated but nonchemotactic A. tumefaciens derivatives were examined for biofilm for

106 erexpression of virB9, virB10, and virB11 in A. tumefaciens did not overcome oncogenic suppression by

107 A. tumefaciens did successfully mobilize IncQ plasmids a

108 ovar II strain, and one biovar III strain of A. tumefaciens displayed between 0.0% and 24.2% tumorige

109 A. tumefaciens donors also mobilized pFRtra to Escherich

110 A. tumefaciens donors transferred a chimeric plasmid tha

111 00, 650, and 250 ug/mL against the growth of A. tumefaciens, E. amylovora, and P. atrosepticum respec

112 A. tumefaciens efficiently transferred this T-DNA into c

113 transformation rates were obtained with the A. tumefaciens EHA101 strain and the pTF101.1 binary vec

114 complementation in a bioR isogenic mutant of A. tumefaciens elucidated that Brucella BioR is a functi

115 ng conserved members of a T4SS, spanning the A. tumefaciens envelope and including a potential pore p

116 an AE, suggesting that the C-terminus of the A. tumefaciens enzyme plays a role in the binding of thi

117 The A. tumefaciens enzyme was found to have the highest rate

118 important for the specificity by F6P in the A. tumefaciens enzyme.

119 ed based on the severe biofilm deficiency of A. tumefaciens exoR mutants.

120 We also show that engineered A. tumefaciens expressing a T3SS can deliver a plant pro

121 can be blocked by infiltrating the leaf with A. tumefaciens expressing RPS2 in the presence of RIN4,

122 A. tumefaciens-facilitated transformation should make po

123 The predicted amino acid sequences of the A. tumefaciens FlaA and FlaB proteins are similar (66% a

124 laC protein reported in R. meliloti, but the A. tumefaciens FlaC is similar in amino acid sequence to

125 FnrN, a second A. tumefaciens FNR-like regulator, is required for induc

126 demonstrated by targeting the pcaHG genes of A. tumefaciens for spontaneous mutation.

127 leaf discs to demonstrate that Osa inhibits A. tumefaciens from transforming these plants to the sta

128 Therefore, the 61 amino acid changes between A. tumefaciens FtsA and R. meliloti FtsA do not prevent

129 When A. tumefaciens FtsA-GFP or R. meliloti FtsA-GFP was expr

130 Overall, this work suggests that A. tumefaciens FtsZ makes distinct contributions to the

131 When R. meliloti FtsZ1-GFP or A. tumefaciens FtsZ-GFP was expressed at low levels in E

132 lls, indicating a requirement for additional A. tumefaciens genes.

133 y, fusion of the N-terminal region of SS4 to A. tumefaciens GS restored the development of wild-type-

134 ent exocellularly on medium on which induced A. tumefaciens had grown and appears as thin filaments o

135 hibiting AP activity in Escherichia coli and A. tumefaciens had junction sites that mapped to two reg

136 We propose that A. tumefaciens has appropriated a progenitor ParA/MinD-l

137 Thus, A. tumefaciens has been critical for the development of

138 tion microscopy to image the localization of A. tumefaciens homologs of proteins involved in cell div

139 on factor of plasmid RP1 (IncPalpha), render A. tumefaciens host cells nearly avirulent.

140 sent in addition to, the BIBAC vector in the A. tumefaciens host.

141 In our study, we utilize the components from A. tumefaciens (i.e. 3-oxooctanyl-l-homoserine lactone [

142 can confer measurable ecological benefits on A. tumefaciens in an environment where the inducing mole

143 hese findings should increase the utility of A. tumefaciens in genetic engineering.

144 ion by the VirA/VirG two-component system in A. tumefaciens in response to various levels of phenolic

145 of the tatABC operons from S.typhimurium or A.tumefaciens in an E.coli tat null mutant strain result

146 st that successful colonization of plants by A. tumefaciens, including T-DNA transfer and opine produ

147 in E. coli and interacted with His-VirB4 in A. tumefaciens, indicating that ATP binding is not requi

148 ex extrachromosomal T-DNA structures form in A. tumefaciens-infected plants immediately after infecti

149 During E. faecalis and A. tumefaciens infection, increased bacterial loads were

150 tion and induce local necrotic lesions in an A. tumefaciens infiltration assay.

151 DNA transfer from A. tumefaciens into plant cells resembles plasmid conjug

152 ations in the chromosomal virulence genes of A. tumefaciens involved in attachment to plant cells hav

153 n alternative respiration, the TAT system of A. tumefaciens is an important virulence determinant.

154 PP and the exopolysaccharide cellulose, when A. tumefaciens is incubated with the polysaccharide stai

155 and LiCl, indicating that the Mrp complex in A. tumefaciens is involved in Na+ circulation across the

156 A. tumefaciens is one of the few organisms with a well c

157 N-(3-oxo-octanoyl)-L-homoserine lactone] of A. tumefaciens is synthesized by the Tral protein, which

158 lic compounds using two wild-type strains of A. tumefaciens, KU12 and A6.

159 A. tumefaciens lacking MdaA accumulates canonical anhydr

160 monstrate that this biocontrol agent targets A. tumefaciens leucyl-tRNA synthetase (LeuRS), an essent

161 he plasmid constructs, transformation of the A. tumefaciens line, and ELISA and Bradford assays to as

162 ed FtsZ1 and FtsA from either R. meliloti or A. tumefaciens localized to the division site in A. tume

163 ens, suggesting that additional gene(s) from A. tumefaciens may be required for the full expression o

164 ns in the genome of transgenic plants during A. tumefaciens-mediated transformation are still poorly

165 The high frequency of A. tumefaciens-mediated transformation via PPO selection

166 dentified that exhibited supersensitivity to A. tumefaciens-mediated transformation when deprived of

167 half of VirB11, associated tightly with the A. tumefaciens membrane, suggesting that both halves of

168 A genetic screen for A. tumefaciens mutants deficient for surface interaction

169 nd visR, activators of flagellar motility in A. tumefaciens, now found to inhibit UPP and cellulose p

170 uA, gguB, or gguC do not affect virulence of A. tumefaciens on Kalanchoe diagremontiana; growth on 1

171 e, strongly suggesting that FtsA from either A. tumefaciens or R. meliloti can bind directly to its c

172 tality of flies inoculated with E. faecalis, A. tumefaciens, or S. aureus.

173 In E. coli, as in A. tumefaciens, ParB repressed the partition operon; Par

174 The A. tumefaciens pathogen hijacks the conserved host infra

175 Thus, although the core architecture of the A. tumefaciens pathway resembles that of C. crescentus t

176 The A. tumefaciens phoB and phoR orthologues could only be d

177 Expression of the A. tumefaciens phoB gene from a tightly regulated induci

178 By using these mutually opposing BphPs, A. tumefaciens presumably has the capacity to simultaneo

179 d against peptide sequences conserved in the A. tumefaciens proton pyrophosphatase, indicated localiz

180 teins encoded by genes of the virB operon of A. tumefaciens pTiC58.

181 t to the putA genes of enteric bacteria, the A. tumefaciens putA gene is not regulated by the PutA pr

182 Transfer of this genetic element from A. tumefaciens R10 requires at least one tra gene found

183 e plasmid carrying the oriT/tra region to an A. tumefaciens recipient at frequencies similar to that

184 t frequencies similar to those observed with A. tumefaciens recipients.

185 Wild-type A. tumefaciens released a rather broad spectrum of autoi

186 To the best of our knowledge, A. tumefaciens represents the first example of profligat

187 Activation of PBAD expression in A. tumefaciens requires a plasmid-borne copy of araC, an

188 oup from anhydromuropeptide chain termini in A. tumefaciens, resolving this apparent anomaly.

189 might be similarly regulated in response to A. tumefaciens responding to host plant stimuli.

190 in lifestyle, such as divisome components in A. tumefaciens resulting from that organism's different

191 on experiments with the genomic replicons of A. tumefaciens revealed that the repABC replicons, altho

192 Transmission electron microscopy of A. tumefaciens revealed the presence of filaments, signi

193 ORFs, including a homolog of cya2, surround A. tumefaciens rnd, but none of these genes exerted a de

194 d culture and are produced at one end of the A. tumefaciens rod-shaped cell in a polar manner.

195 10-fold increase in ipt promoter activity in A. tumefaciens ros mutant strains when compared with wil

196 driven virA and virG in combination with the A. tumefaciens rpoA construct resulted in significant in

197 Availability of the A. tumefaciens sequence will facilitate investigations i

198 A. tumefaciens specific pole-organizing protein (Pop) Po

199 ve was degraded by proteinase K treatment of A. tumefaciens spheroplasts and remained intact upon tre

200 Proteinase K treatment of A. tumefaciens spheroplasts resulted in the disappearanc

201 c maize has been routinely produced using an A. tumefaciens standard binary vector system.

202 droxyacetophenone, similar to what occurs in A. tumefaciens strain A348 from which the virA clone was

203 operons PCR cloned from the genome-sequenced A. tumefaciens strain C58 resulted in complementation ba

204 Here we describe the genome of A. tumefaciens strain C58, which has an unusual structur

205 unts of vir gene inducers, we constructed an A. tumefaciens strain carrying a PvirB-gfp fusion.

206 of the hybrid line Hi II were infected with A. tumefaciens strain EHA101 harboring a standard binary

207 virE2 mutant (the T-DNA donor strain) by an A. tumefaciens strain lacking T-DNA but containing a wil

208 Expression of a cloned avsI gene in A. tumefaciens strain NT1 resulted in synthesis of long-

209 entification of a novel enzyme from the same A. tumefaciens strain, which we named Galactarolactone c

210 lete set of TraR-regulated genes in isogenic A. tumefaciens strains containing an octopine-type or no

211 These engineered A. tumefaciens strains displayed an increased efficiency

212 ich is specifically imported into tumorgenic A. tumefaciens strains to cause cell death.

213 ed in T-pilus biogenesis irrespective of the A. tumefaciens strains used.

214 ely 90% DNA sequence identity across studied A. tumefaciens strains, are required for tumor formation

215 Then, we retransformed these plants with two A. tumefaciens strains: one that allows transient expres

216 in E. coli is less than what is observed in A. tumefaciens, suggesting that additional gene(s) from

217 with the abundance of the mutant proteins in A. tumefaciens, suggesting that VirE2 is stabilized by h

218 that components of the Pho regulon influence A. tumefaciens surface interactions.

219 here biotin synthesis is tightly controlled, A. tumefaciens synthesizes much more biotin than needed

220 Silencing A. tumefaciens T-DNA oncogenes is a new and effective me

221 , two bitopic inner membrane subunits of the A. tumefaciens T-DNA transfer system, in E. coli and hom

222 In vitro, A. tumefaciens T6SS could kill Escherichia coli but trig

223 Crystallization of a proteolytically cleaved A. tumefaciens tadA (missing the last eight amino acids

224 The Ti plasmid-encoded vir genes of A. tumefaciens that are required for T-DNA transfer into

225 Strains of A. tumefaciens that express mutated VirB1 proteins have

226 cts a more fundamental cellular asymmetry in A. tumefaciens that influences and is congruent with its

227 developed on the basis of a double mutant of A. tumefaciens (the DeltabioR DeltabioBFDA mutant), the

228 acter K84 that targets pathogenic strains of A. tumefaciens, the causative agent of plant tumours.

229 division cycle of C. crescentus and that of A. tumefaciens, the functional conservation for this pre

230 These studies suggest that in A. tumefaciens, the Irr protein is most active under low

231 In A. tumefaciens, the level of control afforded is signifi

232 revent VirB2 processing in E. coli, while in A. tumefaciens they result in VirB2 instability, since n

233 er bacteria, c-di-GMP turns down the T6SS in A. tumefaciens thus impacting its ability to compete wit

234 This regulatory system enables A. tumefaciens to express its conjugal transfer regulon

235 rate that VtlR is involved in the ability of A. tumefaciens to grow appropriately in artificial mediu

236 charide may play a role in the attachment of A. tumefaciens to host soma plant cells.

237 We altered EF-Tu in A. tumefaciens to reduce PTI and improved transformation

238 stem (T4SS) and subsequently the capacity of A. tumefaciens to transform plant cells.

239 In A. tumefaciens, TraI, a LuxI-type protein, catalyzes syn

240 nthesis inhibitors cause supersensitivity to A. tumefaciens transformation in three plant species.

241 ation bioassays with two biovar I strains of A. tumefaciens, transgenic Arabidopsis lines averaged 0.

242 A. tumefaciens translocates single-stranded DNA-binding

243 A. tumefaciens translocates the ssDNA-binding protein Vi

244 the cell pole is the site of assembly of the A. tumefaciens type IV apparatus.

245 However, in an in planta coinfection assay, A. tumefaciens used Tde effectors to attack both sibling

246 on, since labeling with [3H]palmitic acid in A. tumefaciens verified that VirB7 is a lipoprotein asso

247 The A. tumefaciens VirB/VirD4 OMCC, solved by transmission e

248 ed of the IMCpKM101 joined to OMCCs from the A. tumefaciens VirB/VirD4, E. coli R388 Trw, and Bordete

249 , and -4) that are 3- to 10-fold larger than A. tumefaciens virB6.

250 The extracellular complementation of an A. tumefaciens virE2 mutant (the T-DNA donor strain) by

251 obacco plants expressing VirE2 protein by an A. tumefaciens virE2 mutant carrying osa confirmed that

252 The GALLS protein can complement an A. tumefaciens virE2 mutant for tumor formation, indicat

253 due to the GALLS gene, which complements an A. tumefaciens virE2 mutant for tumor formation.

254 An A. tumefaciens virE2 virD2DeltaNLS double mutant was abl

255 per plasmids that carry additional copies of A. tumefaciens virulence genes virG and virE were constr

256 w appropriately in artificial medium, and an A. tumefaciens vtlR deletion strain is defective in moti

257 E. coli and the C-terminal 89 residues from A. tumefaciens was able to significantly express virBp::

258 The cellular abundance of these proteins in A. tumefaciens was measured using Western immunoblots an

259 The cell cycle of A. tumefaciens was monitored by time-lapse and superreso

260 t of tumors on plants following infection by A. tumefaciens was optimal at temperatures around 22 deg

261 ytes and also confirmed that no plasmid from A. tumefaciens was present in the sporophyte tissues.

262 ) plasmid by the T-DNA transfer machinery of A. tumefaciens was tested at various temperatures.

263 Using A. tumefaciens, we demonstrated that the detrimental eff

264 Homologous enzymes in P. putida and A. tumefaciens were identified based on a similarity sea

265 s of TraR that were not inhibited by TraM in A. tumefaciens were isolated and fell into two classes.