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

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

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

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

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

20 ive pilus, hereafter called the "T pilus" of 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 glycophorin A blocked T-pilus biogenesis in A. tumefaciens.

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

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

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

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

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

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

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

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

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

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

41 A. tumefaciens also has two additional pleC/divJhomologu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

60 A. tumefaciens attaches efficiently to plant tissues and

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

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

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

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

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

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

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

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

69 The A. tumefaciens C58 genome sequence revealed the presence

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 3 mM DIMBOA is sufficient to block growth of A. tumefaciens completely for 220 hr.

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

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

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

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

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

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

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

101 A. tumefaciens did successfully mobilize IncQ plasmids a

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

103 A. tumefaciens donors also mobilized pFRtra to Escherich

104 A. tumefaciens donors transferred a chimeric plasmid tha

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

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

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

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

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

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

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

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

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

114 A. tumefaciens-facilitated transformation should make po

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 The A. tumefaciens pathogen hijacks the conserved host infra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

184 10-fold increase in ipt promoter activity in A. tumefaciens ros mutant strains when compared with wil

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 A. tumefaciens translocates single-stranded DNA-binding

227 A. tumefaciens translocates the ssDNA-binding protein Vi

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

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

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

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

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

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

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

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

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

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

238 An A. tumefaciens virE2 virD2DeltaNLS double mutant was abl

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

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

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

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

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

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

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

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

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