ライフサイエンスコーパス: c-di-GMP

1 c-di-GMP can assume alternative oligomeric states to eff

2 c-di-GMP caused a persistent increase in cAMP, which sti

3 c-di-GMP interaction leads to active site obstruction, h

4 c-di-GMP interacts with a conserved N-terminal RxxxR mot

5 c-di-GMP interacts with PilZ C-domain motifs 1 and 2 (Rx

6 c-di-GMP is synthesized by diguanylate cyclase (DGC) enz

7 c-di-GMP often regulates the function of its protein tar

8 c-di-GMP production by YfiN was repressed by the peripla

9 c-di-GMP represses the expression of virulence factors i

10 c-di-GMP, a universal bacterial second messenger, can tr

11 While this organism possesses more than 40 c-di-GMP-related enzymes, it remains unclear how signali

12 mutations in alginate production genes and a c-di-GMP regulator gene; while PA01 acquired mutations i

13 CFP) as a biomass indicator and the GFP as a c-di-GMP reporter.

14 tly of Rrp1, suggesting that besides being a c-di-GMP-binding protein, PlzA has other functions.

15 tional and biochemical characterization of a c-di-GMP PDE, PdcA, 1 of 37 confirmed or putative c-di-G

16 ylate (c-di-GMP), by increased activity of a c-di-GMP specific phosphodiesterase.

17 cond messenger 3',5'-cyclic diguanylic acid (c-di-GMP) are involved in regulating transcriptional exp

18 econd messenger, 3-5 cyclic diguanylic acid (c-di-GMP) to the master repressor, BldD.

19 enger molecule 3',5'-cyclic diguanylic acid (c-di-GMP) to transition between these two distinct lifes

20 activated by a 3',5'-cyclic diguanylic acid (c-di-GMP)-regulated transcription factor, MrkH.

21 Additionally, c-di-GMP was found to be localized at the outer boundary

22 Although c-di-GMP is known to stimulate the innate sensor STING,

23 Comparison of apo- and c-di-GMP-bound MrkH structures reveals a large 138 degre

24 onmental regulation of biofilm formation and c-di-GMP signalling.

25 inally, we directly detect elevated pGpG and c-di-GMP in the orn strain.

26 nfirm coupling of the ATPase active site and c-di-GMP binding, as well as the functional significance

27 e regions in apo structure stabilization and c-di-GMP interaction allows distinction between the stat

28 esponse to intracellular DNA, DNA virus, and c-di-GMP.

29 against other cyclic dinucleotides, such as c-di-GMP and cyclic-AMP-GMP, via interactions with both

30 d c-di-GMP-induced cAMP synthesis as well as c-di-GMP-induced stalk gene transcription.

31 of the biofilm and thus represent an average c-di-GMP concentration across the entire biofilm.

32 irulence factors, and suggest a link between c-di-GMP signaling and nutrient availability.

33 -95 alters the binding stoichiometry between c-di-GMP and Alg44 from 2:1 to 1:1.

34 us, as revealed by a telling synergy between c-di-GMP and DIF-1.

35 outcome without undesired cross talk between c-di-GMP-dependent systems.

36 ella enterica and Klebsiella pneumoniae bind c-di-GMP via the domain of unknown function, DUF2819, wh

37 us formation were shown to specifically bind c-di-GMP.

38 -GMP-binding domains, BrlR was found to bind c-di-GMP in vitro at a ratio of one c-di-GMP per two Brl

39 In addition to enhanced BrlR-DNA binding, c-di-GMP levels contributed to PbrlR promoter activity i

40 BldD-(c-di-GMP) sits on top of the regulatory network that con

41 tion necessitates the assembly of the BldD2-(c-di-GMP)4 complex.

42 of coincidence detection that relies on both c-di-GMP and LapG binding to LapD for receptor activatio

43 one component of the protection afforded by c-di-GMP.

44 ation of the ML beta-glucan synthase BgsA by c-di-GMP binding to its C-terminal domain.

45 suggest that the regulation of chemotaxis by c-di-GMP through MapZ orthologs/homologs is widespread i

46 BldD activity is controlled by c-di-GMP concentration and BldO potentially responds to

47 nthesize c-di-GMP, whereas it is degraded by c-di-GMP-specific phosphodiesterases (PDEs).

48 estalk cells reduced stalk gene induction by c-di-GMP, whereas PKA activation bypassed the c-di-GMP r

49 est that the protective response mediated by c-di-GMP is multifactorial, involving chemotactic respon

50 Indeed, domain reorientation by c-di-GMP complexation with MrkH, which leads to a highly

51 ich T4P gene transcription is upregulated by c-di-GMP as a result of its binding to an upstream trans

52 We uncovered three new candidate c-di-GMP receptors in E. coli and characterized one of t

53 In these cases, c-di-GMP-induced cell death was rescued by complementati

54 ly by restoring BrlR production and cellular c-di-GMP levels to wild-type levels.

55 In contrast, reducing cellular c-di-GMP levels of biofilm cells to </= 40 pmol mg(-1) c

56 e biosynthesis genes in response to cellular c-di-GMP.

57 rulence, and confirm the existence of common c-di-GMP signalling pathways that are capable of regulat

58 However, at physiological concentrations c-di-GMP is a monomer and little is known about how high

59 Many bacteria contain c-di-GMP-metabolizing enzymes but lack known c-di-GMP re

60 no acid motifs resembling previously defined c-di-GMP-binding domains, BrlR was found to bind c-di-GM

61 RmcA activity such that the protein degrades c-di-GMP and thereby inhibits matrix production during o

62 terium Azoarcus sp. strain CIB that degrades c-di-GMP in response to aromatic hydrocarbons, including

63 and phosphodiesterases (PDEs) for degrading c-di-GMP.

64 In addition, a CfcR-dependent c-di-GMP boost was observed during this stage in Deltars

65 2 (RxxxR and D/NxSxxG) and a newly described c-di-GMP-binding motif in the MrkH N domain.

66 e intestinal pathogen Clostridium difficile, c-di-GMP inhibits flagellar motility and toxin productio

67 The second messenger cyclic diguanylate (c-di-GMP) controls diverse cellular processes among bact

68 Cyclic diguanylate (c-di-GMP) is a near universal signaling molecule produce

69 and the internal signal cyclic diguanylate (c-di-GMP) is a universal signal that governs the formati

70 n artificial increase of cyclic diguanylate (c-di-GMP) levels in Sinorhizobium meliloti 8530, a bacte

71 The signaling molecule cyclic diguanylate (c-di-GMP) mediates physiological adaptation to extracell

72 The second messenger cyclic diguanylate (c-di-GMP) plays a critical role in the regulation of mot

73 bility landscapes of the cyclic diguanylate (c-di-GMP) riboswitch.

74 of the second messenger, cyclic diguanylate (c-di-GMP), by increased activity of a c-di-GMP specific

75 previously reported that cyclic diguanylate (c-di-GMP), synthesized by diguanylate cyclase A (DgcA),

76 the signalling molecule, cyclic diguanylate (c-di-GMP).

77 the residues required for binding of dimeric c-di-GMP in vitro are also required for efficient algina

78 The cyclic dinucleotide c-di-GMP is a signaling molecule with diverse functions

79 ketide DIF-1 or by the cyclical dinucleotide c-di-GMP.

80 nvolve signaling by the cyclic dinucleotides c-di-GMP and c-di-AMP.

81 y mechanisms of gene expression under direct c-di-GMP control via FleQ and FleQ-like bEBPs.

82 Gac/Rsm network and suggesting that distinct c-di-GMP-modulating signaling pathways can regulate a si

83 NG-dependent host response to cytosolic DNA, c-di-GMP, cGAMP, HIV-1, and DNA viruses.

84 ilm dispersal relies on surprisingly dynamic c-di-GMP concentrations as a result of a sophisticated i

85 Thus, the CFP/GFP ratio gives the effective c-di-GMP per biomass.

86 an EPS biosynthesis gene cluster at elevated c-di-GMP levels.

87 n to be enhanced in the presence of elevated c-di-GMP levels.

88 ge in a manner that is dependent on elevated c-di-GMP levels.

89 via phosphorylation and temporarily elevated c-di-GMP levels.

90 vity in initial attached cells with elevated c-di-GMP levels correlating with increased expression of

91 dA phosphodiesterase mutant producing excess c-di-GMP displays marked attenuation in vitro and in viv

92 port the hypothesis that CelR is a bona fide c-di-GMP synthase and that the nucleotide signal produce

93 sses conserved motifs with high affinity for c-di-GMP binding, the findings here suggest that c-di-GM

94 icating that removal of pGpG is critical for c-di-GMP homeostasis.

95 that MotA-FliG interactions are critical for c-di-GMP-mediated swarming inhibition.

96 A main effector for c-di-GMP signaling in the opportunistic pathogen Pseudom

97 gca- structures to identify target genes for c-di-GMP, and used these genes to investigate the c-di-G

98 ating that cAMP is also the intermediate for c-di-GMP in vivo.

99 ng a prototypical transmembrane receptor for c-di-GMP, LapD, and a cognate periplasmic protease, LapG

100 RxGD motif of the GIL domain is required for c-di-GMP binding, similar to the c-di-GMP-binding I-site

101 next to pssZ, are primarily responsible for c-di-GMP-dependent EPS production.

102 mmary, our results indicate a vital role for c-di-GMP in allowing Brucella to successfully navigate s

103 This is an additional role for c-di-GMP in bacterial physiology.

104 Using flow cells for biofilm formation, c-di-GMP showed a non-uniform distribution across the bi

105 We identified four c-di-GMP turnover enzymes that contribute to increased i

106 R, which is responsible for most of the free c-di-GMP during stationary phase in static conditions.

107 Global c-di-GMP levels were unaffected by spermine supplementat

108 ed by variations in local rather than global c-di-GMP pools.

109 he bacterial second messenger cyclic di-GMP (c-di-GMP) controls biofilm formation and other phenotype

110 The second messenger cyclic di-GMP (c-di-GMP) controls the transition between different life

111 he bacterial second messenger cyclic di-GMP (c-di-GMP) has emerged as a prominent mediator of bacteri

112 Cyclic di-GMP (c-di-GMP) is a widespread second messenger that plays a

113 The cyclic di-GMP (c-di-GMP) second messenger represents a signaling system

114 /LadS/Gac/Rsm network and the cyclic-di-GMP (c-di-GMP) signaling pathways are both central to this ph

115 sition requires activation of cyclic di-GMP (c-di-GMP) synthesis by the Hk1/Rrp1 TCS; B. burgdorferi

116 prokaryotic second messenger cyclic di-GMP (c-di-GMP) to coordinate responses to shifting environmen

117 in response to cytosolic DNA, cyclic di-GMP (c-di-GMP), and DNA viruses.

118 ction of the second messenger cyclic di-GMP (c-di-GMP), which is indispensable for B. burgdorferi to

119 known to require a number of cyclic di-GMP (c-di-GMP)-degrading phosphodiesterases (PDEs) and the ch

120 cellulose production through cyclic di-GMP (c-di-GMP).

121 Cyclic dimeric GMP (c-di-GMP) has emerged as a key regulatory player in the

122 e numerous ways by which cyclic dimeric GMP (c-di-GMP) inhibits motility.

123 erial bis-(3'-5') cyclic GMP (cyclic di-GMP [c-di-GMP]) serves as a second messenger and is involved

124 The complex metabolic pathways governing c-di-GMP synthesis and degradation are highly regulated,

125 els of bis-(3',5')-cyclic-dimeric-guanosine (c-di-GMP), a second messenger that stimulates matrix pro

126 Bis-(3',5') cyclic di-guanylate (c-di-GMP) is a key bacterial second messenger that is im

127 Finally, we show that high c-di-GMP levels affect the localization of a green fluor

128 ficantly reduced cell aggregation under high c-di-GMP conditions.

129 lates the biofilm mode of life, and a higher c-di-GMP concentration reduces cell detachment from biof

130 rovide detailed structural insights into how c-di-GMP controls the activity of an enzyme target indir

131 regulated, but the specific cues that impact c-di-GMP signaling are largely unknown.

132 on: adaptation though incremental changes in c-di-GMP network proteins acquires knowledge from past e

133 h hydrolyze a single phosphodiester group in c-di-GMP to produce 5'-phosphoguanylyl-(3',5')-guanosine

134 Furthermore, this bile-mediated increase in c-di-GMP is quenched by bicarbonate, the intestinal pH b

135 ibit a low-temperature-dependent increase in c-di-GMP, indicating that these DGCs are required for te

136 , including a large set of genes involved in c-di-GMP biosynthesis, degradation, and transmission.

137 letes the picture of all domains involved in c-di-GMP metabolism and reveals that the HD-GYP family s

138 In contrast to numerous enzymes involved in c-di-GMP synthesis and degradation in enterobacteria, on

139 of the primary type IV pilus (T4P) locus in c-di-GMP-dependent cell aggregation.

140 e response regulator domain that resulted in c-di-GMP degradation.

141 d, NicD is dephosphorylated, which increases c-di-GMP levels and leads to phosphorylation and process

142 orn strain could inhibit PDE-As, increasing c-di-GMP concentration.

143 We likewise found that increasing c-di-GMP levels present in planktonic cells to biofilm-l

144 have been ascribed to any of the individual c-di-GMP synthases or phosphodiesterases (PDEs).

145 affect DGC activity of SadC, OdaI inhibited c-di-GMP production by SadC.

146 conformation of the riboswitch that inhibits c-di-GMP binding.

147 n that is induced by binding an intercalated c-di-GMP dimer.

148 44 in complex with dimeric self-intercalated c-di-GMP and characterize its dinucleotide-binding site

149 ng swimming motility or global intracellular c-di-GMP.

150 tent with our prediction, high intracellular c-di-GMP concentration increased transcript levels of T4

151 inosa Deltaorn mutant had high intracellular c-di-GMP levels, causing this strain to overexpress extr

152 imal small intestine, increase intracellular c-di-GMP in V. cholerae.

153 Increased intracellular c-di-GMP concentration in C. difficile was recently show

154 s that contribute to increased intracellular c-di-GMP in the presence of bile acids, and deletion of

155 ndent PDEs, thereby increasing intracellular c-di-GMP in Deltaorn cells.

156 e world-the input stimuli-into intracellular c-di-GMP levels that then regulate genes for biofilm for

157 ad a significant effect on the intracellular c-di-GMP level in P. gingivalis.

158 nd fluorescence was calibrated against known c-di-GMP concentrations.

159 c-di-GMP-metabolizing enzymes but lack known c-di-GMP receptors.

160 with fluorescently and radioisotope-labelled c-di-GMP.

161 P are associated with the biofilm lifestyle, c-di-GMP hydrolysing phosphodiesterases (PDEs) have been

162 erases (PDE-As) end signaling by linearizing c-di-GMP to 5'-phosphoguanylyl-(3',5')-guanosine (pGpG),

163 sterically regulated by GTP, further linking c-di-GMP levels to nutrient availability.

164 ponse than did wild-type Brucella or the low-c-di-GMP guanylate cyclase DeltacgsB mutant.

165 The second messenger c-di-GMP (or cyclic diguanylate) regulates biofilm forma

166 Elevated levels of the second messenger c-di-GMP activate biosynthesis of an unknown exopolysacc

167 response to binding of the second messenger c-di-GMP to a C-terminal extension.

168 trated by the intracellular second-messenger c-di-GMP.

169 ecule, the intracellular secondary messenger c-di-GMP (Bis-(3'-5')-cyclic dimeric guanosine monophosp

170 iofilm cells harbour the secondary messenger c-di-GMP at reduced levels similar to those observed in

171 d expression require the secondary messenger c-di-GMP.

172 ding was enhanced by the secondary messenger c-di-GMP.

173 We also show that temperature modulates c-di-GMP levels in a similar fashion in the Gram-negativ

174 g translating these cues into the modulation c-di-GMP levels to enable dispersion.

175 Cyclic diguanosine monophosphate (c-di-GMP) is a bacterial second messenger that typically

176 Cyclic diguanosine monophosphate (c-di-GMP) is a second messenger that controls diverse fu

177 is-(3'-5') cyclic diguanosine monophosphate (c-di-GMP) phosphodiesterase MbaA.

178 RNA) RsmB, cyclic diguanylate monophosphate (c-di-GMP) and flagellar regulator have been reported to

179 -5')-cyclic-dimeric-guanosine monophosphate (c-di-GMP) acts as an innate immune system modulator.

180 ,5')-cyclic dimeric guanosine monophosphate (c-di-GMP) binding activity post-translationally regulate

181 -5')-cyclic dimeric guanosine monophosphate (c-di-GMP) in cells respiring on nitrate than those grown

182 -5')-cyclic dimeric guanosine monophosphate (c-di-GMP) is a dynamic intracellular signaling molecule

183 ger cyclic di-3',5'-guanosine monophosphate (c-di-GMP) is a key regulator of bacterial motility and v

184 d by cyclic dimeric guanosine monophosphate (c-di-GMP).

185 le PDE gene is sufficient to impact multiple c-di-GMP-dependent phenotypes, including the production

186 ed and synthesized by simplifying the native c-di-GMP structure and replacing the charged phosphodies

187 In search of new c-di-GMP receptors, we screened the Escherichia coli ASK

188 affinity cyclic GMP-AMP (3'3'-cGAMP) but not c-di-GMP or 2'3'-cGAMP.

189 This work also revealed a basal affinity of c-di-GMP-unbound receptor for LapG, the relevance of whi

190 AdVCA0848) that produces elevated amounts of c-di-GMP when expressed in mammalian cells in vivo.

191 of free CheR1, revealed that the binding of c-di-GMP induces dramatic structural changes in MapZ tha

192 We identified a class of c-di-GMP-responsive proteins, represented by the AraC-li

193 review provides an up-to-date compendium of c-di-GMP pathways connected to biofilm formation, biofil

194 Our findings expand the complexity of c-di-GMP signaling in the regulation of the motile-sessi

195 cted that the intracellular concentration of c-di-GMP is low during infection.

196 odulating the intracellular concentration of c-di-GMP.

197 to catalyze the synthesis and degradation of c-di-GMP.

198 ide insights into the molecular evolution of c-di-GMP binding to proteins.

199 ese results suggest that the dimeric form of c-di-GMP represents the biologically active signaling mo

200 demonstrate that the regulatory functions of c-di-GMP-synthesizing DGCs expand beyond surface attachm

201 adation in enterobacteria, only a handful of c-di-GMP receptors/effectors have been identified.

202 be endogenous, as shown by the inability of c-di-GMP to induce cell death in Dictyostelium HMX44A ce

203 ese enzymes eliminates the bile induction of c-di-GMP and biofilm formation.

204 aintain high viability and a higher level of c-di-GMP to reduce cell detachment.

205 As high levels of c-di-GMP are associated with the biofilm lifestyle, c-di

206 Cellular levels of c-di-GMP are controlled through synthesis by GGDEF domai

207 , we recently showed that cellular levels of c-di-GMP are increased in the hyperbiofilm retS mutant.

208 strain with artificially elevated levels of c-di-GMP as well as stimulates swarming in the wild-type

209 searchers discovered that elevated levels of c-di-GMP inhibit swarming by skewing stator selection in

210 conditions by modulating cellular levels of c-di-GMP.

211 action, excess pGpG extends the half-life of c-di-GMP, indicating that removal of pGpG is critical fo

212 Our data suggest a newly identified means of c-di-GMP-mediated control of surface motility, perhaps c

213 Although unrelated in sequence, the mode of c-di-GMP binding to CuxR is highly reminiscent to that o

214 ional data that reveal an unexpected mode of c-di-GMP recognition that is associated with major confo

215 Here, we analyzed the binding mode of c-di-GMP to the allosteric inhibitory site (I-site) of d

216 ines the proposed global and local models of c-di-GMP signaling specificity in bacteria, and attempts

217 s are required for temperature modulation of c-di-GMP levels.

218 ecies harbor separate intracellular pools of c-di-GMP to control different phenotypic outputs associa

219 adenovirus vaccine, fostering production of c-di-GMP as well as proinflammatory responses in mice.

220 Expression profiling of c-di-GMP-regulated genes through the enzootic cycle supp

221 for the in situ, real time quantification of c-di-GMP and show that the amount of this biofilm-regula

222 rent methodologies for the quantification of c-di-GMP are typically based on chemical extraction, rep

223 We found that pGpG reduced the rate of c-di-GMP degradation in cell lysates and inhibited the a

224 identify residues involved in recognition of c-di-GMP.

225 DipA, resulting in the overall reduction of c-di-GMP levels.

226 To determine the role of c-di-GMP in Brucella physiology and in shaping host-Bruc

227 the biofilm, with concentrated hot spots of c-di-GMP.

228 As revealed by the structure of c-di-GMP-complexed FleQ, the second messenger interacts

229 these data confirm that in vivo synthesis of c-di-GMP stimulates strong innate immune responses that

230 de (FMN) variant class, and also variants of c-di-GMP-I and -II riboswitches that might recognize dif

231 egetative growth in a manner that depends on c-di-GMP-mediated dimerization.

232 RsmA also showed a negative impact on c-di-GMP levels in a double mutant DeltarsmIE through th

233 to bind c-di-GMP in vitro at a ratio of one c-di-GMP per two BrlR.

234 In Pseudomonas aeruginosa PA14, c-di-GMP inversely controls biofilm formation and surfac

235 ant at the restrictive temperature prevented c-di-GMP-induced cAMP synthesis as well as c-di-GMP-indu

236 a beta-barrel domain, represents a prototype c-di-GMP receptor.

237 pilA1 is preceded by a putative c-di-GMP riboswitch, predicted to be transcriptionally a

238 GMP PDE, PdcA, 1 of 37 confirmed or putative c-di-GMP metabolism proteins in C. difficile 630.

239 e highly conserved residues markedly reduces c-di-GMP binding and biofilm formation by V. cholerae.

240 pe biofilms and could be induced by reducing c-di-GMP levels via overexpression of genes encoding PDE

241 lms respond to their environment to regulate c-di-GMP concentrations through this sophisticated netwo

242 5-mutagenesis shows that M6 killing requires c-di-GMP-dependent signalling, diverse fungicides and re

243 Restoring c-di-GMP levels to wild-type biofilm-like levels restore

244 at a signalling pathway involving a specific c-di-GMP pool regulated by SagS contributes to the resis

245 d regulatory network that connects the sRNA, c-di-GMP signalling and flagellar master regulator FlhDC

246 ina (PmGH) alone, in complex with substrate (c-di-GMP) and final reaction product (GMP).

247 Diguanylate cyclases synthesize c-di-GMP, whereas it is degraded by c-di-GMP-specific ph

248 on of swimming motility likewise synthesizes c-di-GMP to regulate surface attachment via modulation o

249 protein is both responsible for synthesizing c-di-GMP and involved in biofilm formation and host cell

250 diguanylate cyclases (DGCs) for synthesizing c-di-GMP and phosphodiesterases (PDEs) for degrading c-d

251 response regulator domain, and a C-terminal c-di-GMP phosphodiesterase (PDE) domain.

252 nd biochemical analyses show that tetrameric c-di-GMP links two subunits of BldD through their C-term

253 d for maximal cellulose production, and that c-di-GMP binding is critical for BcsE function.

254 en together, these results demonstrated that c-di-GMP could trigger cell death in Dictyostelium only

255 We show here that c-di-GMP was not sufficient to induce cell death in Dict

256 These data also raise the possibility that c-di-GMP enhances the expression of a subset of RpoS-dep

257 Here, we report that c-di-GMP can assemble into a tetramer that mediates the

258 Proteomics analysis revealed that c-di-GMP regulates several processes critical for virule

259 Here, we show that c-di-GMP binds BldD using an ordered, sequential mechani

260 -GMP binding, the findings here suggest that c-di-GMP can regulate both motility and biofilm formatio

261 The c-di-GMP network has a bow-tie shaped architecture that

262 Additionally, the c-di-GMP-governed auto-aggregation and biofilm phenotype

263 aeruginosa proteins, including BdlA and the c-di-GMP phosphodiesterases DipA, RbdA, and NbdA, have b

264 to residues in the C-domain motif 2 and the c-di-GMP-binding N-domain motif.

265 releasing inhibition of protease LapG by the c-di-GMP effector protein LapD, and resulting in proteol

266 -di-GMP, whereas PKA activation bypassed the c-di-GMP requirement for stalk gene expression.

267 we observed increased transcription from the c-di-GMP-regulated pel promoter.

268 rimetric binding analysis of residues in the c-di-GMP binding site demonstrate that mutation of Arg-1

269 necessary to complete the final step in the c-di-GMP degradation pathway.

270 GMP, and used these genes to investigate the c-di-GMP signal transduction pathway.

271 I)(L/V/I)xxxxLxxxLxxQ that binds half of the c-di-GMP molecule, primarily through hydrophobic interac

272 Binding of the c-di-GMP tetramer by BldD is selective and requires a bi

273 cence protein (GFP) under the control of the c-di-GMP-responsive cdrA promoter (Rybtke, M.

274 cence protein (GFP) under the control of the c-di-GMP-responsive cdrA promoter.

275 The structure shows that the c-di-GMP binding region of Alg44 adopts a PilZ domain fo

276 In this study, we showed that the c-di-GMP-binding protein PlzA, a downstream effector of

277 equired for c-di-GMP binding, similar to the c-di-GMP-binding I-site of the diguanylate cyclase GGDEF

278 ts we propose a mathematical model where the c-di-GMP network is analogous to a machine learning clas

279 gnaling specificity is maintained within the c-di-GMP network.

280 In their c-di-GMP bound conformation Cle proteins interact with t

281 Strikingly, these c-di-GMP-binding motifs also stabilize an open state con

282 This c-di-GMP-binding motif is present in diverse bacterial p

283 enterobacteria is controlled by a two-tiered c-di-GMP-dependent system involving BcsE and the PilZ do

284 ntrol to this cell death and perhaps also to c-di-GMP effects in other situations and organisms.

285 late receptor function and may also apply to c-di-GMP-metabolizing enzymes that are akin to LapD.

286 The 3D structure of MotI bound to c-di-GMP was solved, and MotI-fluorescent fusions locali

287 ond protein domain, after PilZ, dedicated to c-di-GMP-binding.

288 ons and that this activity is fundamental to c-di-GMP signal transduction.

289 ational changes in the receptor that lead to c-di-GMP-dependent protease recruitment.

290 erminator was dose dependent and specific to c-di-GMP binding to the riboswitch aptamer.

291 owth, GcbA itself was found to be subject to c-di-GMP-dependent and growth-mode-specific regulation.

292 utida biofilms, nutrient starvation triggers c-di-GMP hydrolysis by phosphodiesterase BifA, releasing

293 ifies the elusive function of the ubiquitous c-di-GMP network, a key regulator of bacterial social tr

294 This structure reveals a unique c-di-GMP-binding mode, featuring a tandem array of two h

295 e and mechanism of a previously unrecognized c-di-GMP-responsive transcription factor and provide ins

296 redicted to be transcriptionally active upon c-di-GMP binding.

297 ping host-Brucella interactions, we utilized c-di-GMP regulatory enzyme deletion mutants.

298 ity of the signaling network associated with c-di-GMP in P. aeruginosa.

299 protein MapZ cocrystallized in complex with c-di-GMP and its protein target CheR1, a chemotaxis-regu

300 N1-145) from Vibrio cholerae in complex with c-di-GMP at a 1.37 A resolution.