ライフサイエンスコーパス: open complex

1 ter entering and formation of the initiation open complex.

2 is initiated earlier in the pathway, in the open complex.

3 s that ultimately result in formation of the open complex.

4 e bound to P(RM) transition from a closed to open complex.

5 of RNAP with promoter DNA in the closed and open complex.

6 DNA melting and allows the transition to the open complex.

7 sequent steps on the way to formation of the open complex.

8 e region that becomes single-stranded in the open complex.

9 moter complex to a transcriptional competent open complex.

10 se pairs near the initiation site to form an open complex.

11 x but bent more sharply by 86 degrees in the open complex.

12 romoter opening or to stabilize a productive open complex.

13 A did not affect dissociation rates from the open complex.

14 and the highest for the constructs mimicking open complex.

15 y interactions of RNA polymerase with DNA in open complex.

16 erization of a closed promoter complex to an open complex.

17 the leuV promoter that is unwound within the open complex.

18 in vitro, indicating destabilization of the open complex.

19 duplex DNA promoter to form a pre-initiation open complex.

20 n 1.1 differs dramatically in holoenzyme and open complex.

21 uggesting their role in stabilization of the open complex.

22 tween the enzyme and the promoter DNA in the open complex.

23 2, 2, 3, and 4 are similar in holoenzyme and open complex.

24 t as a key player directing formation of the open complex.

25 sely interacts with the promoter only in the open complex.

26 tro by decreasing the lifetime of the rrn P1 open complex.

27 he transcription start site, as in the final open complex.

28 into a catalytically competent RNAP-promoter open complex.

29 oter, is not limited by the stability of the open complex.

30 nwinds promoter DNA to form an RNAP-promoter open complex.

31 eam double-stranded DNA of the RNAP-promoter open complex.

32 ization of the initial closed complex to the open complex.

33 bent DNA results in the catalytically active open complex.

34 DksA for RNAP decreases almost 10-fold in an open complex.

35 rt varsigma(54) closed promoter complexes to open complexes.

36 of the formation of RNA polymerase-promoter open complexes.

37 its amino acids are used to form functional open complexes.

38 promoters like rrnB P1 that make short-lived open complexes.

39 gy ppGpp, generally decrease the lifetime of open complexes.

40 owly and were much longer-lived than rrnB P1 open complexes.

41 isomerises into transcriptionally competent open complexes.

42 ng interconversions between the dead-end and open complexes.

43 lpha subunits in transcriptionally competent open complexes.

44 s on the intrinsic catalytic capacity of the open complex and also on the partitioning between produc

45 Both the open complex and an abortive complex containing a short

46 s in region 1.2 can affect promoter binding, open complex and initiated complex formation and the tra

47 a plays an essential role in stabilizing the open complex and interacts specifically with the N-termi

48 The low temperature-trapped open complex and its isothermally formed state are shown

49 s in the TRTG motif of amyP destabilized the open complex and prevented the maintenance of open compl

50 econstituted PICs, indicating a destabilized open complex and shift to the closed/PIN state.

51 , the detailed mechanism of formation of the open complex and the high resolution structures of these

52 that is close to the promoter spacer in the open complex and to the upstream boundary of the transcr

53 omoter DNA but only undergo transition to an open complex and transcription initiation when acted on

54 achieve promoter escape nevertheless formed open complexes and extended bubbles, which collapsed bac

55 s show an unexpected architecture of minimal open complexes and the regulation of activity by TFIIF a

56 attempts for each successful formation of an open complex, and efficient release of sigma(54) from th

57 containing the lambdaP(R) promoter, form an open complex, and initiate transcription in a temperatur

58 interacts with the rRNA backbone only in the open complex, and the R53E substitution enhanced initiat

59 otides there is a distribution of closed and open complexes, and the promoter DNA is bent slightly by

60 Open complexes are committed to transcription, suggestin

61 and quantified the overall bend angle in the open complex as well as in the +3 abortive complex: a be

62 howed a smaller amount of the pre-initiation open complex at equilibrium, indicating that the individ

63 A, preventing RNA polymerase from forming an open complex at nlpAp.

64 eplication by inhibiting the formation of an open complex at the replication origin, thus elucidating

65 o KMnO(4) indicated that in about 20% of the open complexes at 20 degrees C the DNA strands are not f

66 contrast, ppGpp decreased the half-lives of open complexes at all promoters, whether the half-life w

67 led kinetic analysis in vitro indicated that open complexes at amino acid promoters formed much more

68 pen complex and prevented the maintenance of open complexes at low temperatures.

69 and forked DNA, similar to the formation of open complexes at promoters, is a multistep process, and

70 , remodel the polymerase so that it can form open complexes at promoters.

71 ur mutant enzymes are shown to form unstable open complexes at the lambdacro promoter.

72 lymerase (RNAP), leading to the formation of open complexes at the promoter.

73 R) promoter, it does prevent it from forming open complexes at this promoter.

74 ription factor form an initiation-competent "open" complex at a promoter by disruption of about 14 ba

75 oters region 1.1 stimulates the formation of open complexes; at the P(minor) promoter, region 1.1 inh

76 To form a functional open complex, bacteriophage T7 RNA polymerase (RNAP) bin

77 Formation of the strand-separated, open complex between RNA polymerase and a promoter invol

78 yme couple ATP hydrolysis to formation of an open complex between the promoter and RNA polymerase.

79 Formation of the stable, strand separated, 'open' complex between RNA polymerase and a promoter invo

80 it catalyzes ATP-dependent formation of the open complex, but also in efficient promoter escape, whe

81 at subtle changes in the conformation of the open complex can profoundly affect its function.

82 GreA effects on rrnB P1 open complex conformation reveal a new feature of GreA d

83 ce of nucleotides: a dead-end complex and an open complex, constituting a branched interaction pathwa

84 in the size of the transcription bubble: the open complex contains a 10.4 +/- 0.1 bp bubble, while th

85 e overall equilibrium constant for closed to open complex conversion is 0.5 and the net rate of open

86 te, and Bpa cross-linking to map the path of open complex DNA at amino acid and nucleotide resolution

87 NAP binding to the promoter and formation of open complexes do not reflect a large-scale qualitative

88 ransient state kinetic studies show that the open complex, ED(o), is formed via an intermediate ED(c)

89 This complex isomerizes to an open complex, ED(o1), in an energetically unfavorable re

90 e ED(o1) further isomerizes to a more stable open complex, ED(o2), with a rate constant around 300 s(

91 F unexpectedly modulates the activity of the open complexes, either repressing or stimulating initiat

92 Thus, eIF2beta anchors eIF1 and TC to the open complex, enhancing PIC assembly and scanning, while

93 sA in vitro, including shifting the promoter-open complex equilibrium in the dissociation direction,

94 eavage pattern reveals structures similar to open complex, except for notable changes to region 3 of

95 We find that the scrunched open complex exhibits reduced abortive product synthesis

96 D helicases involved in promoter melting and open complex extension.

97 Open complexes form in a concerted manner at pflgM, whil

98 The defect in pre-initiation open complex formation affected downstream steps such as

99 hibit replication, while monomers facilitate open complex formation and activate the ori.

100 rgenic region, we have demonstrated in vitro open complex formation and activation of transcription i

101 on of the upstream footprint did not require open complex formation and also occurred in reactions in

102 sed on their ability to increase the rate of open complex formation and decrease the rate of promoter

103 a DNase I footprint downstream of Mor due to open complex formation and generation of a second footpr

104 SutA appears to affect intermediates in the open complex formation and its N-terminal tail is requir

105 urface-exposed residues in the regulation of open complex formation and promoter DNA binding to be be

106 These data refine the structural model for open complex formation and reveal a novel interaction in

107 en sigma(2) and the DNA during both promoter open complex formation and sigma(70)-dependent early elo

108 moter binding properties and low-temperature open complex formation are similar for pfliC, pfliD, and

109 However, the rate of open complex formation at P(R-GA) in vitro was roughly o

110 We have examined the kinetics of open complex formation at the lacP1 promoter using trypt

111 ffects the RNA polymerase-mediated closed to open complex formation at the rob promoter.

112 as an ideal probe to measure the kinetics of open complex formation because its fluorescence is sensi

113 Analysis of open complex formation by a three-step pathway that incl

114 develop the first quantitative model of the open complex formation by bacterial RNAP.

115 rwinding the operator-promoter DNA to permit open complex formation by pre-bound RNA polymerase.

116 o drive conformational changes necessary for open complex formation by sigma(54)-RNA polymerase.

117 are required for NorR-dependent catalysis of open complex formation by sigma(54)-RNAP holoenzyme (Esi

118 e ATPase domain to oligomerize and stimulate open complex formation by the s54 form of RNA polymerase

119 g--to activator and ATP hydrolysis-dependent open complex formation by the sigma(54)-RNAP.

120 de of bacterial sporulation and inhibits the open complex formation due to steric clash with sigma re

121 has been implicated in the stabilization of open complex formation during nucleotide excision repair

122 rigin, ATP hydrolysis may be unnecessary for open complex formation facilitated by His-pi.F107S.

123 d suggests that DnaD and DnaB do not require open complex formation for the stable association with D

124 The kinetics of promoter binding and open complex formation in bacteriophage T7 RNA polymeras

125 P enhances RNA polymerase binding as well as open complex formation in both promoters.

126 hese variants retain the ability to activate open complex formation in vitro.

127 of the dMyx action and a stepwise pathway of open complex formation in which core enzyme mediates the

128 Our results show that open complex formation is completely dependent on FNR an

129 nal energy source is used and the energy for open complex formation is derived from the free energy o

130 te that the linking number change induced by open complex formation is essentially all due to bubble

131 omplex conversion is 0.5 and the net rate of open complex formation is nearly 150 s(-1).

132 the template at position +2, the process of open complex formation is nearly complete.

133 , with both factors present, the kinetics of open complex formation is significantly faster than in t

134 udies reveal that the nucleotide that drives open complex formation needs to be a triphosphate and to

135 nner at pflgM, while a sequential pattern of open complex formation occurs at pfliD.

136 substitutions for Y430 and W433 also affect open complex formation on promoter DNA lacking the -11A

137 The results suggest that open complex formation only occurs efficiently on replac

138 s also demonstrate that ATP and pi stimulate open complex formation over a wide range of temperatures

139 The dynamics of open complex formation provides unique insights into the

140 We derive how the open complex formation rate depends on DNA duplex meltin

141 Open complex formation requires both transcription facto

142 nitiation pathway provides insights into how open complex formation steps that are sensitive to the p

143 rates also depend on the kinetics following open complex formation such as initial nucleotide incorp

144 ding and the observed rate of pre-initiation open complex formation that corresponds to the sum of DN

145 tor re-organises the centre to favour stable open complex formation through adjustments in sigma(54)-

146 NA polymerase binding and directly stimulate open complex formation to activate transcription.

147 e (T429A) results in the largest decrease in open complex formation yet observed for any single subst

148 (CR) in terms of the three step mechanism of open complex formation yields the equilibrium constant K

149 o, His-pi.F107S-dependent local DNA melting (open complex formation) occurs in the absence of host pr

150 (R), the mutation with the largest effect on open complex formation, --10G (T:A --> G:C), substantial

151 , using permanganate footprinting to measure open complex formation, and DNase I footprinting to moni

152 e RNA polymerase alpha subunit is needed for open complex formation, and we describe two experiments

153 ects of the substitutions on the kinetics of open complex formation, as well as on the ability of the

154 d for an open intermediate on the pathway to open complex formation, in which these 2-APs are no long

155 I and the DNA fork junction structure during open complex formation, is communicated to the AAA activ

156 tics reveals longer lasting states preceding open complex formation, suggesting enhanced supercoiling

157 olymerase, remains competent for stimulating open complex formation, suggesting that this DNA superco

158 rent conformations adopted by the DNA during open complex formation, we investigated the contribution

159 igin of plasmid R6K, yet monomers facilitate open complex formation, while dimers, the predominant fo

160 consider a more complex two-step view of the open complex formation.

161 sequences of the promoter, thus facilitating open complex formation.

162 e of an isomerization step on the pathway to open complex formation.

163 NA binding determinants of polymerase during open complex formation.

164 nce enhanced both RNA polymerase binding and open complex formation.

165 Its ATPase activity is required for open complex formation.

166 mally associated with stable DNA melting and open complex formation.

167 d to overcome the sigma(54)-imposed block on open complex formation.

168 -RNA polymerase-DNA interactions that favour open complex formation.

169 uorescence increase is assigned to the final open complex formation.

170 or RNA polymerase sequence on the process of open complex formation.

171 enzymes were observed prior to and including open complex formation.

172 Ps affect the kinetics and thermodynamics of open complex formation.

173 e -35 element, consequently facilitating the open complex formation.

174 37 to intercalate and distort the DNA during open complex formation.

175 AP base at -4 from the guanine at -5, during open complex formation.

176 oriV, do not bind stably and fail to induce open complex formation.

177 ancer binding activator protein to stimulate open complex formation.

178 nication pathway linking changes in sigma to open complex formation.

179 the abrB and rrnB1 promoters and facilitates open complex formation.

180 responsible for the DksA-specific effects on open complex formation.

181 f coiled-coil tip interactions with RNAP for open complex formation.

182 oduction of the first phosphodiester bond is open complex formation.

183 e pair disruption during the early stages of open complex formation.

184 on and increases the recruitment of RNAP and open complex formation; (ii) the distal UP subsite plays

185 n filament and the subsequent restoration of open-complex formation as the central mechanism of count

186 Specifically, the kinetics of open-complex formation can be explained by a model where

187 pstream promoter DNA, or both on the rate of open-complex formation with promoters that lack UP eleme

188 ation requires the melting of DNA to form an open complex, formation of the first few phosphodiester

189 le the unstable, transcriptionally competent open complexes formed at ribosomal promoters.

190 Open complexes formed at the three mutant promoters are

191 The open complexes formed by the mutant and wild-type RNAPs

192 ing effect observed in bandshift analysis of open complexes formed on this set of constructs provided

193 Dissociation kinetics of open complexes formed with DeltaJAW RNAP and/or DT+12 DN

194 egion (TATA to TAAA) decreased the extent of open complex generated at equilibrium.

195 The open complex half-life was up to 26-fold shorter in the

196 rties of the DNA bubble in the transcription open complex have been characterized by topological anal

197 NA bubble, creating the relatively unstable (open) complex I(2).

198 , which rapidly converts to much more stable open complexes (I(3), RP(o)).

199 k of transition from the intermediate to the open complex, identifying the sigma subunit as a key pla

200 s for the structure of DNA in the functional open complex in solution, and provide an important compl

201 me and the bacterial RNA polymerase-promoter open complex in solution.

202 and initiates the formation of a prepriming open complex in the absence of DnaA protein.

203 formation of the preinitiation open complex (open complex in the absence of initiating nucleotide).

204 e probing shows that the conformation of the open complex in the presence of CRP appears qualitativel

205 ormation of a fully open initiation complex (open complex in the presence of the initiating nucleotid

206 ator prevents RNA polymerase from forming an open complex in vitro.

207 sed complex, which is then converted into an open complex in which the promoter is both sharply bent

208 (RNAP) and double-stranded promoter DNA, to open complexes, in which the enzyme is able to access th

209 disrupting eIF2alpha contacts favored in the open complex increase initiation at suboptimal sites, an

210 amyP TRTG motif dramatically stabilizes the open complex intermediate during transcription initiatio

211 Formation of a transcriptionally competent open complex is a highly regulated multistep process inv

212 Formation of the open complex is a multi-step process during which transi

213 However, a question of how the open complex is formed still remains open, and several q

214 Our results suggest that once the open complex is formed, TFIIH decays into an inactive co

215 Even though the open complex is less stable in the mutant promoters, the

216 that the conformation of RNAP present in an open complex is not optimal for DksA binding and that DN

217 nary activator--RNA polymerase--aer promoter open complex is organized differently from complexes at

218 indicate that the melted template DNA in the open complex is positioned to bind the +2 NTP.

219 model for the overall path of the DNA in the open complex is presented that is consistent with the me

220 the formation of transcriptionally-competent open complexes is affected by changing the length of the

221 s previously been shown to exhibit different open complex kinetics and stabilities relative to Escher

222 ectly by reducing the lifetime of the rrn P1 open complex, liberating enough RNAP to stimulate transc

223 In vitro, DksA binds to RNAP, reduces open complex lifetime, inhibits rRNA promoter activity,

224 ed, resulting in a 4- to 30-fold decrease in open complex longevity at an rRNA promoter and a approxi

225 ement for DNA unwinding, reminiscent of the 'open complex' model of RNA polymerase-promoter DNA inter

226 ition of +1 NTP alone does not stabilize the open complex; nor is it required for +2 NTP binding.

227 ree-dimensional architecture of the complete open complex (OC) composed of the promoter DNA, TATA box

228 o investigate roles of the discriminator and open complex (OC) lifetime in transcription initiation b

229 Formation of the RNA polymerase II (Pol II) open complex (OC) requires DNA unwinding mediated by the

230 te of the RNA polymerase (RNAP), forming the open complex (OC).

231 nges increase lifetimes of lambdaPR and T7A1 open complexes (OCs) by >10(5)-fold and >10(2)-fold, res

232 h is not sufficient to melt and stabilize an open complex of a non-specific DNA.

233 Isomerization of a closed to open complex of a promoter upon RNA polymerase binding i

234 her stringent promoters investigated so far, open complex of rrnB P1 has been shown to be intrinsical

235 location and size of the DNA bubble in this open complex of the mtRNAP closely resembles that of the

236 The single-stranded region of DNA within the open complex of transcriptionally active genes provides

237 te an 8-oxoG template started from partially open complexes of pol beta.

238 Stable open complexes of Pol II are largely absent from the tra

239 nformation of promoter DNA in the closed and open complexes of T7 RNAP.

240 er, Rpo41 alone was able to form a competent open complex on a pre-melted promoter.

241 promoter melting and/or stabilization of the open complex on LSP.

242 In contrast to other efflux conduits, the open complex only displays a slight preference for catio

243 t inhibit the formation of the preinitiation open complex (open complex in the absence of initiating

244 helix, as expected, and a relatively mobile "open complex" or undocked state.

245 del where nucleotide selection occurs in the open complex prior to the formation of a closed ternary

246 rving as a "molecular mimic" of DNA, but, in open complex, region 1.1 is located outside the active c

247 The conversion into open complexes requires the ATPase activity of activator

248 d bubbles, which collapsed back to closed or open complexes, resulting in repeated futile scanning.

249 under conditions that favor formation of the open complex results in destabilization of the preinitia

250 nges to form the transcriptionally competent open complex RP(o).

251 formation of the transcriptionally competent open complex (RP(o)) by Escherichia coli RNA polymerase

252 ase (R) and promoter DNA (P) that create the open complex (RP(o)).

253 conformational changes required to form the open complex (RP(O)).

254 bble" within a catalytically active RNAP-DNA open complex (RP(o)).

255 but is required to form stable RNAP-promoter open complexes (RP(o)) and is essential for viability in

256 or conversion of closed complexes (RP(c)) to open complexes (RP(o)) but do not affect K(B), the equil

257 ate a burst of I(2) by rapidly destabilizing open complexes (RP(o)) with 1.1 M NaCl.

258 rmation of this transcriptionally competent "open" complex (RP(o)) by Escherichia coli RNAP at the la

259 of the open region to form the highly stable open complex, RP(o).

260 ne another, to produce a polymerase/promoter open complex (RPo) competent for transcription.

261 nwinds promoter DNA to form an RNAP-promoter open complex (RPo) containing a single-stranded 'transcr

262 bp of promoter DNA, forming an RNAP-promoter open complex (RPo) containing a single-stranded transcri

263 ficant effect of Sp1 on the apparent rate of open complex (RPo) formation (k2) or on the apparent rat

264 Mechanistic analyses of promoter open complex (RPo) formation establish that RbpA and Car

265 in the catalytically competent RNAP-promoter open complex (RPo).

266 the approach by showing that the DNA path in open complexes (RPO) is the same as in high-resolution X

267 and show that RbpA stabilizes RNAP-promoter open complexes (RPo) via a distinct mechanism from that

268 5 base pairs of the promoter DNA to form an 'open' complex; scanning downstream to a transcription st

269 However, in the rrnB P1 open complex, scrunching occurs before RNA synthesis beg

270 great flexibility in the position of active open complexes, spanning 30 to 80 bp downstream from TAT

271 The kinetics and open-complex stabilities of CarD mutants further clarify

272 n shown to be intrinsically unstable, making open complex stability a potential regulatory step in tr

273 reported on the energetics of CarD-mediated open complex stabilization on the Mycobacterium tubercul

274 stigate the function and architecture of the open complex state of RNA polymerase II (Pol II), Saccha

275 domain, thereby allowing acquisition of the open complex status.

276 mation of the RNA polymerase (RNAP)-promoter open complex step to the productive elongation complex s

277 1 preinitiation complexes, presumably at the open complex step, contributes prominently to transcript

278 ivity, implying that it is predominantly the open complex that is sensitive.

279 cts with eIF1 and Met-tRNAi exclusive to the open complex that should destabilize the closed state.

280 We find that in stable DeltaJAW open complexes the downstream boundary of hydroxyl radic

281 In this initial unstable "open" complex the template strand appears correctly posi

282 To generate the open complex, the conserved catalytic core of the RNAP c

283 in bacteria, including the formation of the open complex, the reaction of initial transcription, and

284 ator form shifts the interactions toward the open complex to activate transcription.

285 site, pronounced in the promoter DNA of the open complex, was not present.

286 enerate the pre-initiation DNA bubble in the open complex, we estimate that one half (3.5-4 kcal mol(

287 Here, using a fluorescent reporter of open complex, we quantitate RPo formation in real time a

288 I (Pol II), Saccharomyces cerevisiae minimal open complexes were assembled by using a series of heter

289 on formation of transcriptionally competent open complexes were studied by DNAse I footprinting, KMn

290 ssays using DNA probes that mimic closed and open complexes were used to explore the determinants of

291 ce establish the transcriptionally competent open complex, where full promoter melting occurs.

292 DnaA promoted the formation of the DnaA-oriC open complex, which leads to DNA replication over-initia

293 IC resulted in quantitative conversion to an open complex, which retained all 31 proteins, contrary t

294 9 degrees +/- 7 degrees was measured for the open complex, while a bend of 47 degrees +/- 11 degrees

295 and Promoter) is melted from -4 to +1 in the open complex with all three proteins and from -4 to +3 w

296 s, i.e. open and closed, of apoFgFCO1 and an open complex with product fucose at atomic resolution.

297 potentiating the formation of the productive open complex with RNA polymerase.

298 Probing of the architecture of the minimal open complexes with TFIIB-FeBABE [TFIIB-p-bromoacetamido

299 dicates that when polymerase is in a stable (open) complex with P(minor), the DNA is single stranded

300 inds to free GK (super-open) and GK-glucose (open) complexes with comparable affinities (Kd = 0.23 +/