# # Creator RegulonDB Database # schemeURI http://regulondb.ccg.unam.mx/ # affiliation Center for Genomics Science # Title Dataset of sentences with Regulatory Interactions (RIs) and Growth Conditions (GCs) # titleType Title # Publisher Program of Computational Genomics, CCG # PublicationYear 2018 # ResourceType Genomics data # resourceTypeGeneral Dataset # Rights http://regulondb.ccg.unam.mx/menu/download/full_version/terms_and_conditions.jsp # Format text # Version v1.0 # Language en # keywords regulatory interaction, automatic classification, passage detection, information extraction, bionlp # relatedIdentifier https://www.ncbi.nlm.nih.gov/pubmed/?term=24903516 # relatedIdentifierType URL # relationType References # Contributor RegulonDB Team # ContributorType ContactPerson # ContactPersonURI http://regulondb.ccg.unam.mx/menu/about_regulondb/contact_us/index.jsp # ContactPersonEmail regulondb@ccg.unam.mx # Contributor Carlos-Francisco Méndez-Cruz # ContributorType Researcher # Contributor Julio Collado Vides # ContributorType Researcher # Contributor Cecilia Ishida-Gutiérrez # ContributorType Curator # Description # # The file contains a list of validated sentences where Regulatory Interactions (RIs) and Growth Conditions (GCs) can be found. # Each line is one sentence with at least one RI and GC, and more than one sentence can be found in the same reference. # Tokenization, and sentence split was performed by OntoGene text mining system (http://www.ontogene.org/) # # Columns: # Column 1: PMID reference used to get the sentence with al least one Regulatory Interaction (RI) and Growth Condition (GC). # Column 2: ID of sentence assigned by OntoGene. # Column 3: Manual validated sentence where the information about the RI and GC is found. # Column 4: Class, RI+GC = with Regulatory Interaction and Growth Condition. # # 9409145 202 In the absence of arabinose , AraC protein represses expression of the araBAD and araC promoters ( called P araBAD and P araC , respectively ) ( 62 , 99 , 114 , 117 , 144 – 146 , 156 , 157 , 165 ) . RI+GC 9409145 203 With arabinose , AraC activates transcription from the promoters of the catabolic operons ( Fig . 3 ) . RI+GC 9409145 310 Transcription initiation from P melAB is stimulated by the MelR regulator with melibiose . RI+GC 9409145 530 Effects of S and the transcriptional activator AppY on induction of the Escherichia coli and cbdAB - appA operons in response to carbon and phosphate starvation . RI+GC 9409145 1172 Genetic definition of the Escherichia coli zwf “ Soxbox , ” the DNA binding site for SoxS - mediated induction of glucose 6 - phosphate dehydrogenase in response to superoxide . RI+GC 9409145 2306 SmtB is a metal - dependent repressor of the cyanobacterial metallothionein gene smtA : identification of a Zn inhibited DNA - protein complex . RI+GC 24272778 9 We demonstrate arabinose - dependent repression of ydeNM by AraC , in contrast to the well - described arabinose - dependent activation of other target genes . RI+GC 24272778 16 E . coli AraC activates transcription of the araBAD , araFGH , araE , and araJ transcripts in the presence of its inducer , L - arabinose ( 5 ) . RI+GC 24272778 213 Thus , ydeNM is a novel AraC - regulated operon that is directly repressed by AraC in an arabinose - dependent manner . RI+GC 24272778 328 Specifically , we identified AraC binding sites that ( i ) repress rather than activate transcription in an arabinose - dependent manner ( ydeN ) , ( ii ) result in little or no observed regulation under standard laboratory growth conditions ( ytfQ and dcp ) , and ( iii ) are located within a gene ( dcp ) . RI+GC 24272778 349 Although arabinose - dependent repression by AraC has not been observed before , there are clear parallels with arabinose - dependent activation of araBAD transcription . RI+GC 24272778 351 At the araC - araBAD intergenic region , AraC forms a repression loop in the absence of arabinose due to the dimerization of distally bound AraC monomers . RI+GC 24272778 360 ygeA and polB are positively regulated by AraC and arabinose due to partial read - through of Rho - independent terminators ( Fig . 2 , 4 , and 5 ) . RI+GC 21890697 8 ArgP mediates lysine ( Lys ) repression of argO , dapB , and gdhA in vivo , for which two alternative mechanisms have been identified : at the dapB and gdhA regulatory regions , ArgP binding is reduced upon the addition of Lys , whereas at argO , RNA polymerase is trapped at the step of promoter clearance by Lys - bound ArgP . RI+GC 21890697 10 All were repressed upon Lys supplementation , and in vitro studies demonstrated that ArgP binds to the corresponding regulatory regions in a Lys - sensitive manner ( with the exception of argO , whose binding to ArgP was Lys insensitive ) . RI+GC 21890697 16 ( That E . coli gdhA may be under ArgP control had also been suggested earlier [ 33 ] . ) In addition , in vitro studies have suggested that ArgP activates the transcription of the dnaA and nrdA genes that are involved in DNA metabolism and replication ( 20 , 27 – 29 ) . RI+GC 21890697 30 Stable recruitment by ArgP of RNA polymerase to the argO promoter is observed in the presence of Arg or Lys , following which the two coeffectors exert dramatically opposite effects in the ternary complex ; whereas productive transcription from the argO promoter is stimulated in the presence of ArgP and Arg , RNA polymerase is trapped at the promoter at a step after open complex formation in the presence of ArgP and Lys ( 26 ) . RI+GC 21890697 41 Our results indicate that negative regulation involving Lys as coeffector is mediated by ArgP and that the target genes include argO , lysP , lysC , asd , dapB , dapD , lysA , and gdhA . RI+GC 21890697 124 Recently , Ruiz et al . ( 41 ) had also independently identified ArgP ’ s role both as a transcriptional activator and in mediating the repression of the lysP gene by Lys . RI+GC 21890697 125 However , they reported that ArgP binds the lysP regulatory region with similar affinities in both the absence and presence of Lys and had accordingly suggested that ArgP mediates Lys repression of lysP by the same mechanism of RNA polymerase trapping that it does at argO . RI+GC 21890697 126 Since our results were different from those of Ruiz et al . ( 41 ) , we repeated the EMSA experiments with lysP , using a graded series of ArgP concentrations in the absence or presence of Lys ( Fig . 2A ) ; the data clearly establish that binding of ArgP to the lysP template is Lys sensitive . RI+GC 21890697 161 In EMSA experiments using ArgP and the cis regulatory regions of both dnaA and nrdA , we observed binding at an apparent K d of around 150 nM that was unchanged in the presence or absence of Lys ( Fig . 3 and Table 4 ) . RI+GC 21890697 168 In the case of argO , ArgP mediates its transcriptional activation by Arg , as well as its repression by Lys ( 7 , 26 , 32 , 37 ) ; the latter is achieved by a mechanism involving the active trapping at the argO promoter by ArgP of RNA polymerase , which is then prevented from being released to engage in productive transcription ( 26 ) . RI+GC 21890697 171 These include lysP , lysC , lysA , dapD , and asd ( in addition to argO , dapB , and gdhA ) , all of which exhibited ArgP - mediated repression upon Lys supplementation in vivo , as well as ArgP binding to the corresponding cis regulatory regions in vitro . RI+GC 21890697 211 While this work was being completed , Ruiz et al . ( 41 ) independently reported the identification of lysP as a Lys - repressed transcriptional target of ArgP . RI+GC 9537375 35 In this study , we show for the first time that the operator sequence is indeed the binding site for the negative regulator GntR and that gluconate is the true inducer of gntT , by inactivation of GntR binding to the operator . RI+GC 9537375 121 To investigate the role of the CRP and adenylate cyclase in catabolite repression of the gntT gene by glucose and gluconate , crp and cya null mutations were transduced into the strain carrying the chromosomal gntT : : lacZ fusion . RI+GC 8655507 225 An excellent CAP - binding site ( 19 ) is centered at bp 70 with respect to the transcriptional start site of the gntK gene , explaining the phenomenon of glucose catabolite repression observed in Northern blot analysis . RI+GC 12618441 14 These results led us to propose that GntH activates GntII and represses the GntI genes in the presence of metabolites derived from gluconate , allowing the organism to switch from the GntI to the GntII system . RI+GC 12618441 114 COLI 1787 Downloaded from http : / / jb . asm . org / FIG . 2 — Continued . on January 11 , 2016 by Instituto de Biotecnologia , UNAM the gntK expression was repressed by GntR in the absence of gluconate . RI+GC 12618441 229 Taken together , GntH seems to repress the expression of the gntKU and gntT genes , and the repression occurs even in the presence of gluconate , which could be physiologically important , as discussed below . RI+GC 12618441 314 In contrast to the case for GntR , the GntI genes in the presence of cloned GntH were negligibly induced by gluconate ( Table 3 ; Fig . 5 ) . RI+GC 12618441 324 Notably , GntH was able to repress the GntI genes even in the presence of gluconate . RI+GC 12618441 332 In the model , gluconate is first imported by gluconate permease , GntP , as demonstrated ( 15 ) , and interacts with the GntR molecule to induce the GntI system genes . RI+GC 12618441 344 The products 5 - ketogluconate and idonate bind to GntH , resulting in activation of the GntII genes and repression of the GntI genes . RI+GC 12618441 345 Finally , gluconate depletion inside the cell leads to the repression of the GntI genes by GntR again . RI+GC 12618441 348 The production of GntH may repress the GntI genes by forming a complex with 5 - ketogluconate or idonate and further induce GntII genes , whereas GntR molecules are being released from the operators in the state of interacting with gluconate . RI+GC 8636021 168 The ability of MarA to autoactivate the mar promoter was studied as a function of time following induction by salicylate . RI+GC 7836283 154 OmpR can activate or repress the ompF gene depending on osmolarity conditions and the strength of the promoter ( 30 ) . RI+GC 19376854 13 waaY expression was also regulated by MarA ( multiple - antibiotic resistance regulator ) , which shares a binding site ( soxbox ) with SoxS , and was induced by salicylate , a nonoxidative compound . RI+GC 19376854 246 waaY promoter is also induced by antibiotics through the mar system . RI+GC 14701822 86 After a 1 - h induction of MarA by IPTG , a decline was seen in the levels of transcripts of purA ( Fig . 1A ) and hdeA ( Fig . 1B ) . RI+GC 14701822 165 The purA promoter is repressed by PurR in the presence of purines ( 32 ) , and the promoter of hdeA is repressed by HN - S ( 33 ) . RI+GC 12100559 36 Liochev and colleagues ( Liochev et al . , 1999 ) have shown that the activity of NfsA was induced by exposure to paraquat in a SoxR - dependent fashion and therefore nfsA was also a member of the soxRS regulon . RI+GC 12100559 140 Additionally , although induction of chromosomal marA in wild - type cells by sodium salicylate caused a clear upregulation of nfnB expression , identical concentrations of 2,2 ´ - dipyridyl ( 5 mM ) , recently reported as an inducer of the chromosomal Rob ( Rosner et al . , 2002 ) , failed to demonstrate such an effect . RI+GC 12100559 143 For instance , Rob has been shown to bind and activate the zwf promoter in vitro but whole cell zwf regulation cannot be activated by Rob , although the gene responds to SoxS and MarA ( Ariza et al . , 1995 ; Jair et al . , 1995 1996a ; b ) . RI+GC 12067348 21 marA expression is repressed by MarR and is derepressed by the interaction of MarR with various phenolic compounds such as salicylate . RI+GC 12067348 22 soxS expression is activated by an oxidized form of SoxR produced by treating cells with the superoxide - generating agent paraquat ( Demple , 1996 ) . RI+GC 11601842 90 For example , both the AcrAB efflux pump and micF induced - decreases in OmpF porin are turned on in response to oxidative stress or weak acids . RI+GC 11601842 142 Lrp plays a major role in transcriptional repression of micF when cells are in nutrient poor media . RI+GC 11601842 153 SoxR is a sensor protein activated by oxidative stress and in turn it transcriptionally activates soxS . RI+GC 2543976 65 Although MetJ and AdoMet have little effect on the synthesis of MetH ( line 1 vs . line 3 ) , they inhibit the expression of the metE gene by 75 % ( line 1 vs . line 3 ) . RI+GC 2543976 66 The addition of MetJ and AdoMet to incubations containing MetR also results in a 75 % inhibition of metE expression but no effect on MetH expression ( line 2 vs . line 4 ) . RI+GC 2543976 73 If the MetR protein synthesized from pRSE562 was responsible for the observed increase in MetH synthesis , the MetJ protein and AdoMet , if added to the first incubation , should inhibit the increase by preventing MetR synthesis . RI+GC 2543976 142 One explanation for this discrepancy is that the purified MetR protein ( 20 ) may be partly inactive so that the amount needed for activation of metE and metH expression in vitro appears higher than actually required . RI+GC 11139621 176 Binding of NagC and Mlc to nagE operators in vivo As Mlc showed a stronger affinity for the nagE operator than NagC , it seemed possible that Mlc might be able to regulate the nagE promoter in the absence of NagC in vivo . ThreenagE – lacZ fusions were tested : the standard ‘ loop - forming ’ nagBE – lacZ fusion , whose expression is repressed by NagC binding co - operatively to the nagE and nagB operators ; and two single operator nagE – lacZ fusions , missing the nagB promoter / operator , but carrying the same nagE – lacZ junction . RI+GC 11139621 188 To verify that Mlc does bind preferentially to the nagE operator in vivo , the effect of plasmids overproducing either Mlc or NagC was tested in a strain mutated for both mlc and nagC . Plasmids expressing either NagC or Mlc produce considerable repression of the nagBE – lacZ looped fusion , reducing expression 88 - and 56 - fold ( Table 2 ) . RI+GC 11139621 340 ( 1998 ) A global repressor ( Mlc ) is involved in glucose induction of the ptsG gene encoding major glucose transporter in Escherichia coli . RI+GC 7565112 12 Therefore , expression of nuo is regulated by O2 and nitrate via ArcA , NarL , FNR and IHF at sites within the - 277 region , and by other factors including C4 dicarboxyiates at a site between - 277 and - 899 . RI+GC 7601827 117 RESULTS Maximal nitrate repression of pfl expression is dependent on functional NarL , NarP , NarX , and NarQ proteins . RI+GC 7601827 217 For example , nitrate induction of the narGHJI operon ( 21 ) and the narK gene ( 12 ) is controlled exclusively by NarL , while induction of the fdnGHI operon is controlled principally by NarL , but NarP also effects a degree of control ( observed with a narL mutant ) ( 21 ) . RI+GC 7601827 218 Expression of the dmsABC and the frdABCD operons is repressed in the presence of nitrate , and this repression is dependent on the NarL protein ( 8 , 10 , 21 , 28 ) . RI+GC 7601827 267 The mechanism which the cell employs to repress pfl expression with nitrate clearly involves NarL and NarP , but a further factor ( s ) which dictates whether repression is strong or weak , perhaps in response to the intracellular redox status , must be involved . RI+GC 7854119 8 Summary Expression from both the Escherichia coli nir and nrf promoters is dependent on anaerobic induction by FNR but is further reguiated by NarL and NarP in response to the presence of nitrite and nitrate in the growth medium . RI+GC 7854119 11 The nrf promoter can be activated by either NarP or NarL in response to nitrite but is repressed by NarL in response to nitrate . RI+GC 7854119 185 The resuits in Tabie 7 confirm that expression from pnrf was totally FNR dependent and induced during anaerobic growth . RI+GC 8437517 14 Mutations in the putative NarL - binding site at the nirB promoter decrease FNR - dependent anaerobic induction , suggesting that NarL acts as a helper to FNR during transcription activation . RI+GC 8437517 23 NarL , wiiicin was initiaily discovered as a transcription factor essentiai for the activation of nitrate reductase expression by nitrate ( Stewart , 1982 ) , Recent studies of the nitrate reductase promoter have identified the FNR - and NarLbinding sites around 41 and 200 bp upstream of the transcription start , respectiveiy ( Li and DeMoss , 1988 ; Walker andDeMoss , 1991 ; Dong ef a / . , 1992 ) . RI+GC 10537212 12 This latter result indicated that ArcA suppresses anaerobic hyb expression and that a further factor , which remains to be identified , is involved in controlling anaerobic induction of operon expression . RI+GC 10537212 116 In the narL narP double null mutant , nitrate repression of hyb expression was relieved and anaerobic regulation after growth in the absence of nitrate was similar to that observed in the wild - type strain ( Table 3 ) . RI+GC 10537212 205 Unlike the Arc system , DpiAB is functional in aerobically growing cells and the DpiA protein acts to repress appY gene expression during aerobiosis . RI+GC 10537212 253 Effects of s and the transcriptional activator AppY on induction of the Escherichia coli hya and cbd – appA operons in response to carbon and phosphate starvation . RI+GC 11004182 11 While either NarL or NarP was able to induce nrfA - lacZ expression in response to low levels of nitrate , only NarL could repress at high nitrate levels . RI+GC 11004182 27 Expression of the nrfABCDEFG operon ( previously described as aeg - 93 [ 3 ] ) and the nirBDC operon is elevated during anaerobic cell growth by the Fnr regulatory protein ( 1 , 10 , 14 ) . RI+GC 11004182 28 The addition of nitrite , but not nitrate , is reported to further elevate nrfA expression via either the NarL or NarP response regulators . RI+GC 11004182 29 In contrast , NarL is reported to repress nrfA expression in response to nitrate , whereas NarP cannot ( 14 – 16 , 23 , 24 ) . RI+GC 11004182 31 In contrast , only NarL is reported to activate nirB in response to nitrite ( 23 , 24 ) . RI+GC 11004182 105 From prior batch culture experiments , both NarL and NarP were reported to activate nirB - lacZ in response to nitrate ( 23 , 24 ) . RI+GC 11004182 106 The chemostat experiments ( Fig . 3A ) also demonstrate that NarL or NarP can function independently of each other to induce nirB expression in response to nitrate . RI+GC 11004182 130 During batch cell culture conditions , nitrite was reported to induce nrfA expression via either the NarL or NarP response regulator proteins , while only nitrate was reported to cause repression of nrfA expression and only by NarL ( 14 , 16 , 24 ) . RI+GC 11004182 139 First , either NarL or NarP can activate nrfA - lacZ expression in response to added nitrate . RI+GC 11004182 140 Second , NarL can repress nrfA - lacZ expression when nitrate is present , whereas NarP cannot ( compare the NarL NarP strain to the NarL NarP strain and to the wild - type strain ) . RI+GC 11004182 143 These findings therefore require a reexamination of the regulatory models based on batch culture studies wherein NarL or NarP can activate nrfA expression in response to nitrite only ( 24 ) . RI+GC 11004182 278 The Fnr protein ( F ) induces nrfA operon expression under anaerobic conditions . RI+GC 11004182 308 During anaerobiosis , the Fnr protein ( F ) binds at its consensus recognition site , centered at 42 , to activate nirB operon expression . RI+GC 12079504 4 Expression of the dmsABC genes that encode the membrane - associated DMSO / TMAO reductase is positively regulated during anaerobic conditions by the Fnr protein and negatively regulated by the NarL protein when nitrate is present . RI+GC 12079504 6 Mutations within the Fnr site that deviated from the wild type sequence , TTGATaccgAACAA , or that removed an entire half - site , either impaired or abolished the anaerobic activation of dmsA - lacZ expression . RI+GC 12079504 26 These studies define the molecular interactions of Fnr and NarL at the dmsABC P1 promoter that together provide for the oxygen and nitrate regulated expression of this respiratory pathway operon . RI+GC 12079504 27 Results and Discussion Effect of cis - acting mutations in the Fnr binding site on anaerobic induction of dmsA - lacZ expression To investigate the effects of sequence changes in the dmsA Fnr - recognition site on the anaerobic activation of dmsAlacZ expression , site - directed mutagenesis and β - galactosidase assays were performed ( Figure 1 ) . RI+GC 12079504 29 A 3 - fold increase in anaerobic activation of dmsA - lacZ expression was observed for the consensus Fnr site ( 300 - fold ) relative to the 114 - fold anaerobic activation by Fnr seen for the native dmsA sequence ( Figure 1 , λJA303 and λJA250 , respectively ) . RI+GC 12079504 31 To our knowledge , this " consensus " Fnr - dependent dmsA promoter exhibits the highest anaerobic induction of any Fnr - regulated E . coli promoter examined . RI+GC 12079504 33 Likewise , the poor match of the Fnr site at the promoter for the fumarate reductase gene , frdA to the consensus Fnr sequence may account for the relatively weak anaerobic induction for this respiratory operon [ 14 ] . RI+GC 12079504 38 When a two base - pair change was introduced into the left Fnr halfsite ( e . g . , TTGAT to TTAGT ) of the native dmsA sequence , it nearly abolished the anaerobic induction of dmsA - lacZ expression ( Figure 1 , λJA257 ) . RI+GC 12079504 41 To evaluate how the spacing between the Fnr binding site and the start of dmsA transcription alters the anaerobic activation of dmsA - lacZ expression , single basepair insertions were introduced at position - 35 ( λJA448 and λJA449 ) . RI+GC 12079504 42 The 114 - fold anaerobic activation seen for the wild - type dmsA promoter was reduced to about 35 - fold in each of the two mutants ( Figure 1 ) , indicating that the position of the Fnr site at the wild - type dmsA promoter is important for controlling optimal dmsA gene expression . RI+GC 12079504 59 Location of NarL binding sites at the dmsA promoter Under anaerobic conditions , dmsA expression is repressed approximately 10 - fold by NarL when nitrate is present [ 4 ] . RI+GC 12079504 102 In addition , β - galactosidase assays revealed that the 10 - fold nitrate dependent repression of dmsA - lacZ expression was unaffected by the deletion of upstream DNA sequence to - 71 relative to the start of dmsA transcription , further pinpointing the location of the 5 ' end of the NarL recognition site for dmsA ( data not shown ) . RI+GC 12079504 106 Finally , a similar hydroxyl radical footprint pattern of 8 – 9 protected regions of 3 – 4 bp spaced 10 nucleotides apart was also observed for NarLphosphate at the promoter region of the frdA gene , another anaerobically induced gene that is repressed by NarL in the presence of nitrate ( data not shown ) . RI+GC 12079504 137 + 40 + 30 + 20 + 10 + 1 - 10 - 20 - 30 - 40 - 50 dmsA Conclusions This study investigated the effects of sequence changes in the Fnr - recognition site on the anaerobic activation of dmsA - lacZ expression as well as examined the NarL recognition sites within the dmsABC regulatory region . RI+GC 12079504 138 The data illustrates that Fnr is responsible for the 100 - fold anaerobic activation of dmsA expression . RI+GC 12586421 241 ( 2002 ) The NorR protein of Escherichia coli activates expression of the £ avorubredoxin gene norV in response to reactive nitrogen species . RI+GC 12923080 26 The nitrate induction of fdnG expression occurs at the level of transcription control , where NarL is a strong activator and NarP is a weak activator ( 11 , 20 ) . RI+GC 12923080 163 The effect of NarP on nitrate - dependent repression of fdnG - lacZ expression was not observed in batch cultures since5080 WANG AND GUNSALUS J . RI+GC 12923080 169 The nitrate - dependent repression of fdhF - lacZ expression shown in Fig . 3B was confirmed by batch culture experiments in which NarL negatively regulated gene expression . RI+GC 12923080 226 NarP thus performs a unique role to fine - tune fdnG operon expression by delaying the ability of NarL to activate when nitrate levels are low . RI+GC 12923080 238 However , according to the current model , when nitrate is also present , the NarL regulatory protein is activated , and NarL phosphate then binds to the fdhF upstream region to suppress expression . RI+GC 12923080 290 However , in the presence of a high formate concentration , FHLA binds to the UAS region to activate fdhF gene expression . RI+GC 13129959 9 The napF operon control region exhibits unusual organization of DNA binding sites for the transcription regulators Fnr and NarP , which activate transcription in response to anaerobiosis and nitrate , respectively . RI+GC 13129959 184 In the 146 strain , which retains the ModE protein binding site , ( napF - lacZ ) expression was induced during growth with added molybdate , and this induction required the modE allele ( data not shown ) . RI+GC 13129959 230 Likewise , the phospho - NarP protein , but not the phospho - NarL protein , in conjunction with the Fnr protein , activates in vitro transcription from the napF P1 promoter ( 10 ) . RI+GC 15667305 11 Nitrate - and nitriteinduced transcription from the hcp promoter was activated by the response regulator proteins NarL and NarP . RI+GC 15978080 11 Summary Expression from the Escherichia coli nrf operon promoter is activated by the anaerobically triggered transcription factor , FNR , and by the nitrate / nitrite ioncontrolled response regulators , NarL or NarP , but is repressed by the IHF and Fis proteins . RI+GC 15978080 18 Hence , Fis protein is a major factor responsible for catabolite repression at the nrf promoter , and Fis can override activation by FNR and NarL or NarP . RI+GC 15978080 317 Binding of Cra protein to a site centred at position - 16.5 represses the nir promoter when cells are in minimal medium ( Tyson et al . , 1997 ) . RI+GC 7643383 8 Expression of the aeg - 46.5 operon NY 14853 - 8101 , USA ( anaerobically expressed gene at 46.5 minutes on the genetic map ) is induced during anaerobic growth by the global transcriptional regulatory protein Fnr . RI+GC 7643383 9 aeg - 46.5 operon expression is further induced by the NarP protein in response to nitrate or nitrite and this induction is antagonized by NarL . RI+GC 7643383 12 A sequence with similarity to the Fnr - binding site consensus , centered at position 64.5 , was essential for Fnr - dependent anaerobic induction of aeg - 46.5 operon expression . RI+GC 7643383 36 Nitrate and nitrite induction of the nirB operon and nitrite induction of nrfA operon expression is mediated to differing extents by the NarL and NarP proteins ( Rabin & Stewart , 1993 ; Tyson et al . , 1993 , 1994 ) . RI+GC 7643383 43 Previous experiments suggest that the nitrate and nitrite induction of aeg - 46.5 operon expression is mediated solely by the NarP protein , in contrast to all other nitrate and / or nitrite - inducible operons studied to date that are efficiently activated by the NarL protein alone or by both the NarL and NarP proteins ( Rabin & Stewart , 1993 ) . RI+GC 7643383 44 The NarP - dependent nitrate and nitrite induction of aeg - 46.5 operon expression is increased in a narL null strain . RI+GC 7643383 83 Also , the effects of control region deletions from 275 to 68 on the nitrate and nitrite induction ratios of aeg - 46.5 operon expression ( Table 1 ) may be an indirect result of the effect on Fnr - dependent regulation . RI+GC 7643383 95 Thus , it appears that the NarL protein can weakly induce aeg - 46.5 operon expression in response to nitrate . RI+GC 7643383 187 These results confirm that occupancy of heptamers 40 and 49 by the NarP protein is essential for efficient nitrate and nitrite induction of aeg - 46.5 operon expression . RI+GC 7643383 227 A NarP / NarL site centered at – 44.5 bp Our results demonstrate that the symmetrical region centered at position 44.5 ( Choe & Reznikoff , 1993 ) is essential for NarP - dependent nitrate and nitrite activation of aeg - 46.5 operon expression . RI+GC 7643383 266 In an anaerobic environment the Fnr protein ( F ) is active and binds to the – 64.5 site to induce aeg - 46.5 operon expression . RI+GC 8501030 15 We found that the primary signal for NarP - dependent aeg - 46.5 operon induction is nitrite rather than nitrate . RI+GC 8501030 154 These results show that the NarP protein activates F ( aeg - 46.5 - lacZ ) expression in response to nitrate and nitrite and that the NarL protein antagonizes this activation . RI+GC 8631699 185 However , repression in the presence of oxygen or nitrate was significantly reduced with respect to the monocopy fusion , which suggests that an increase in the copy number of caiF renders transcription of the gene less dependent on the anaerobic regulators FNR and NarL . RI+GC 9335308 147 Nitrate and nitrite induction of cydD is dependent on NarL and Fnr . RI+GC 9335308 207 The dps promoter is activated by OxyR during growth and by IHF and s in stationary phase . RI+GC 9852003 12 The dcuB gene is strongly activated anaerobically by FNR , repressed in the presence of nitrate by NarL , and subject to cyclic AMP receptor protein ( CRP ) - mediated catabolite repression . RI+GC 9852003 45 Expression of fumB is also induced anaerobically ( 1.5 - or 5 - fold ) in a manner which is dependent on both FNR and ArcA ( 41 , 44 ) . RI+GC 9852003 59 The results show that the dcuB gene is expressed exclusively under anaerobic conditions in a manner that is FNR dependent and that it is repressed by NarL in the presence of nitrate and is subject to CRP - mediated catabolite repression . RI+GC 9852003 183 This demonstrates that NarL has the major role in nitrate - induced repression of dcuB expression ( Fig . 5Dii ) . RI+GC 9852003 286 The dcuB gene is expressed exclusively under anaerobic conditions in a manner that is largely FNR dependent , is repressed by nitrate through a mechanism that is mostly NarL mediated , and is strongly induced by C 4 - dicarboxylates anaerobically . RI+GC 15995204 56 Additionally , nitrate , acting via the NarL response regulator , represses the transcription of the frdA and dcuB - fumB operons ( Fig . 1C ) ( 18 , 22 , 27 , 53 ) . RI+GC 15995204 198 This indicates that the NarX - NarL system is solely responsible for nitrate repression of these four operons ( dcuB - fumB , aspA , frdABCD , and dcuSR ) involved in fumarate respiration . RI+GC 15995204 217 More recently , the DcuS - DcuR regulatory system has been identified as mediating dicarboxylate - responsive activation of frdA operon transcription ( 17 , 67 ) . RI+GC 15995204 222 Expression from a monocopy ( dcuS - lacZ ) operon fusion revealed three - to fourfold repression by nitrate ( Table 2 ) , virtually all of which can be attributed to the NarX - NarL regulatory system rather than the paralogous NarQ - NarP system ( data not shown ) . RI+GC 16261196 189 In agreement with these findings , the nitrate - and nitrite - induced transcription from the hcp promoter in E . coli was found to depend on the response regulator proteins NarL and NarP [ 45 ] . RI+GC 17449618 193 A major protection mechanism against NO in the cytoplasm is provided by flavorubredoxin and its reductase , NorVW , which are synthesized in response to NO activation of the transcription activator NorR ( 15 , 20 , 22 ) . RI+GC 17449618 535 The NorR protein of Escherichia coli activates expression of the flavorubredoxin gene norV in response to reactive nitrogen species . RI+GC 19245365 12 NarLdependent activation at both the yeaR and ogt promoters is decreased in rich medium and this depends on Fis , a nucleoidassociated protein . RI+GC 19245365 187 Thus we propose that , under conditions where Fis levels are raised , Fis binds at the yeaR promoter and prevents nitrate - dependent induction by blocking NarL binding to its target ( illustrated in Figure 6A ) . RI+GC 19245365 203 In ( B ) and ( C ) , the hypersensitive site at position 76 that is induced by NarL binding to NarL I is marked with a star , and the Fis - induced hypersensitive site at position 90 is marked by a filled circle . results confirm that the ogt promoter is induced by NarL in response to nitrate ions , without help from FNR . RI+GC 19245365 231 We suggest that the induction of ogt by NarL alone in response to external nitrate provides a prophylactic insurance policy against possible genotoxic effects arising from nitrate metabolism . RI+GC 10850996 36 E - mail : m . h . j . bennik @ ato . wag - ur . nl . have shown that overexpression of Rob ( or its N - terminal domain alone ) activates transcription of sodA ( encoding manganese - containing superoxide dismutase ) , fumC ( encoding fumarase C ) , inaA ( encoding a weak acid - inducible protein ) , and micF ( gene for an antisense RNA repressing the outer membrane porin OmpF ) . RI+GC 10850996 216 Other genes reported to be activated by Rob in vitro ( fpr , fumC , micF , nfo , sodA , and zwf ) ( 15 ) or by Rob overexpression in vivo ( fumC , inaA , micF , and sodA ) ( 5 ) were not found in our study ; thus , it appears that the mutagenesis and screening procedure was not saturating . RI+GC 10850996 224 Rob overproduction elicited the strongest transcriptional activation of ybaO and aslB ( 15 - to 20 - fold ) . RI+GC 20023096 13 We found that this repression is AraC dependent and involves a mechanism where arabinose - bound AraC binds to the xylose promoters and represses gene expression . RI+GC 20023096 46 We found that this repression is AraC dependent and is most likely due to binding by arabinose - bound AraC to the xylose promoters , with consequent inhibition of gene expression . RI+GC 20023096 117 When bound with arabinose , AraC activates the transcription of the araBAD , araE , and araFGH operons and represses transcription from the araC operon . RI+GC 20023096 211 Based on our results with the arabinose transporter deletion strains , arabinose likely inhibits xylose gene expression by one of two mechanisms : either ( i ) arabinose - bound AraC binds to the P xylA promoter and prevents it from being activated by xylose - bound XylR or ( ii ) arabinose directly binds XylR and inhibits its activity . RI+GC 8980677 32 Model of AraC induction by L - arabinose at the araBAD promoter ( P BAD ) , according to Lobell & Schleif ( 1990 ) . RI+GC 1560456 11 AraC protein bound at the aral site immediately adjacent to the RNA polymerase binding site of the pBAX ) promoter stimulates transcription of the araBAD genes in the presence of arabinose ( Lee et al . , 1974 ; Hahn et al . , 1986 ; Martin et al . , 1986 ) . RI+GC 8516313 35 When arabinose is added , the subunit that formerly contacted araO2 releases and shifts to the araI2 half - site , from which it activates transcription from the araBAD promoter ( PBAD ) ( 19 ) , results that extend a prior observation that the presence of arabinose can extend the region of aral2 that AraC protects from DNase I digestion ( 20 ) . RI+GC 3041410 19 In the presence of arabinose , AraC protein bound at the araI site , which is immediately adjacent to the RNA polymerase binding site of the PBAD promoter , stimulates transcription of the araBAD genes ( Fig . 1 ) . RI+GC 1744033 132 The facts that arabinose induces the substantial transcription of araJ messenger ( 11 ) and that this transcription is regulated by CAP and AraC ( 11 , 18 ) are , however , consistent with araJ actually being translated and serving some purpose in the arabinose metabolism of E . coli . RI+GC 1447222 17 In the presence of arabinose , AraC protein activates the expression of the araBAD , araFGH , and araE promoters ( 6 - 10 ) . RI+GC 1447222 18 In the absence of arabinose , AraC protein negatively regulates the transcription of the araBAD operon . RI+GC 1447222 19 It has been proposed that araFGH and araE are also negatively regulated by AraC protein in the absence of arabinose ( 9 ) . RI+GC 1447222 27 In the absence of arabinose , AraC protein represses araBAD transcription by a mechanism involving cooperative binding of AraC protein to two AraC binding sites at a distance , resulting in formation of a DNA loop ( 15 - 19 , 39 , 40 ) . RI+GC 6262769 126 The binding of the CAP alone , in the absence of P2 , activates Pc but not PBAD , At the conclusion of this work , we learned of the model for araC and araBAD regulation proposed by Ogden et aL ( 12 ) , who located two sites on ara DNA for the binding of CAP and two sites for the binding of araC protein . RI+GC 19906180 54 ArgP is able to bind the argO control region by itself , but arginine is required to stimulate transcription whereas lysine counteracts this effect ( Laishram and Gowrishankar , 2007 ) . RI+GC 19906180 65 Results Lrp stimulates argO expression in a leucine - sensitive manner The fact that Lrp affects the expression of many genes involved in the metabolism and transport of amino acids , including the artPIQM operon involved in arginine uptake ( Hung et al . , 2002 ; Tani et al . , 2002 ; Cho et al . , 2008 ) , and our interest in establishing a coherent global picture of the regulation of arginine metabolism in E . coli ( Caldara et al . , Fig . 2 . Histogram presentation of b - galactosidase activities measured in cell - free extracts of an E . coli strain FW102 ( WT ) and its isogenic lrp : : Tn10 disruption mutant ( lrp : : Tn10 ) bearing a single - copy F - P argO – lacZ fusion . RI+GC 19906180 138 DNase I footprinting of Lrp binding to the argO control region ( top strand revealed ) without and with 7 mM L - leucine in the binding buffer . RI+GC 19906180 170 The role of endogenous arginine in ArgP - mediated activation of P argO on minimal medium is corroborated by the higher promoter activity in the DargR background ( 2.4 - fold ) which is hardly further increased by exogenous arginine ( Fig . 6 ) . RI+GC 19906180 205 According to the classification of Cho et al . ( 2008 ) , argO belongs to the category of genes that are regulated in a reciprocal manner by Lrp and leucine , i . e . RI+GC 19906180 207 Interestingly , many other transporters for amino acids such as the uptake genes for arginine ( artPIQM ) , serine ( sdaC ) , alanine ( cycA ) and proline ( proY ) , and the export gene for leucine ( leuE ) are also regulated reciprocally by Lrp and leucine ( Kutukova et al . , 2005 ; Cho et al . , 2008 ) . RI+GC 19906180 209 In contrast , several transporters for aromatic amino acids ( brnQ , ilvKHMGF and ilvJHMGF ) appear to be regulated by the concerted mode , their expression is downregulated by Lrp and leucine potentiates this effect ( Cho et al . , 2008 ) . RI+GC 19906180 220 In the absence of ArgP , both the affinity of Lrp for the argO control region and its concentration in the cell would be sufficiently high to ensure Lrp - mediated activation of P argO , even in the presence of excess leucine . RI+GC 19906180 228 The modulation of ArgP - mediated activation of P argO by arginine and lysine ensures that the exporter is only synthesized in significant amounts in conditions of both high arginine and low lysine concentrations ( and not when both concentrations are high ) . RI+GC 17504942 4 Laishram and Jayaraman Gowrishankar 1 Laboratory of Bacterial Genetics , Centre for DNA Fingerprinting and Diagnostics , Hyderabad 500076 , India In vivo transcription of the Escherichia coli argO gene , which encodes an arginine ( Arg ) exporter , requires the LysR - family regulator protein ArgP ( previously called IciA ) and is induced in the presence of Arg or its naturally occurring antimetabolite analog canavanine . RI+GC 17504942 22 In vivo studies with argO - lac fusions have established that argO is under the strict transcriptional control of ArgP ( a member of the LysR family of regulator proteins [ Schell 1993 ] ) , and that its expression is induced by 1 mM Arg as well as by its toxic analog canavanine ( CAN , which is a plant derived naturally occurring antimetabolite ) ( Nandineni and Gowrishankar 2004 ) . RI+GC 17504942 37 Our results indicate that whereas ArgP activates argO transcription in the presence of Arg through the process of RNA polymerase ( RNAP ) recruitment ( Ptashne and Gann 1997 ; Browning and Busby 2004 ) , the mechanism by which Lys addition phenocopies an argP mutation is not simply by preventing the binding of ArgP to the argO operator but instead by reversible trapping of the recruited RNAP at the promoter in a novel molecular complex that is proficient for neither productive nor abortive transcription . RI+GC 17504942 57 ( RO ) Run - off transcript from argO promoter ; ( EE ) end - to - end transcription product ; ( His ) histidine . those from the in vivo studies in that they demonstrated ( 1 ) a basal level of argO transcription in the absence of ArgP ( Fig . 1C , lane 1 ) , ( 2 ) substantial ArgP - dependent activation occurring in presence of Arg or CAN but not Lys ( Fig . 1C , cf . lanes 3,5 and 1,2,4 ) , and ( 3 ) reversal of such activation upon addition of Lys but not of a nonspecific amino acid such as histidine ( Fig . 1C , cf . lanes 6 and 7 ) . RI+GC 18502871 151 There is a strict correlation between the presence of ArgP and a high level of lysine - repressed dapB transcription , provided that the dapB regulatory region contains the necessary cis - acting upstream sequences . RI+GC 18502871 152 Interestingly , lysine is known to virtually abolish transcription activation of argO , a bona fide ArgP target . RI+GC 15150242 191 ( iii ) The transcription of yggA in vivo is ArgP dependent and is induced by exogenous Arg or Arg - Ala ( and also by an argR mutation ) , whereas the addition of Lys or Lys - Ala phenocopies the effect of an argP null mutation ; furthermore , yggA expression is rendered constitutive in an argP d strain . RI+GC 15150242 194 Therefore , a straightforward interpretation of our results , as further discussed below , is that ( i ) ArgP is a transcriptional activator of yggA , ( ii ) ArgP ’ s activator function is enhanced by Arg and inhibited by Lys , and ( iii ) yggA encodes an Arg ( and CAN ) exporter in E . coli . RI+GC 21441513 322 ArgP of E . coli is also responsible for the lysine - dependent regulation of dapB , which encodes one of the enzymes of the diaminopimelate and lysine biosynthesis pathway ( 2 ) , and argO , which encodes the arginine exporter ArgO ( 24 , 30 ) . RI+GC 15066032 129 The role of CAP in induction Expression of the chbB – lacZ fusion during growth on glycerol was only slightly higher than that on glucose in the wild - type strain , which is not typical of a cAMP / CAP - regulated gene ( Table 1 ) . RI+GC 15066032 168 Further evidence that growth on chitin is limiting for induction of NagC is shown by the analysis of the effect of chitin and chitobiose on induction of a NagC - regulated nagB – lacZ fusion . RI+GC 18028317 31 In the presence of chitobiose , ChbR , along with CRP , activates transcription from the chb promoter ( Plumbridge and Pellegrini , 2004 ) . RI+GC 10601201 180 The CRP K52N mutant possesses a third activating region , designated AR3 ( small black triangle ) , that has been proposed to contact the subunit ( see text ) . contrast to CRP , which effectively activated the wild - type fucPIK promoter only in the presence of fucose but failed to activate the IS5 - disrupted promoter in the presence or absence of fucose , as previously reported ( 8 ) . RI+GC 15659677 8 P1 controls eda induction on gluconate and is regulated by GntR . RI+GC 15659677 9 P2 controls eda induction on glucuronate and galacturonate and is regulated by KdgR . RI+GC 9657988 164 Interestingly , eda is also a member of the KdgR regulon and is induced approximately fourfold by growth on glucuronate ( 20 ) . RI+GC 14593252 6 The results presented allow us to speculate that GntR initiates expression of the GntII genes , followed by their large induction by GntH when cells were grown in gluconate minimum medium . RI+GC 14593252 28 Bausch et al . [ 1998 ] provided biochemical evidence that the idnD and idnO genes in GntII encode idonate dehydrogenase , oxidizing idonate to 5 - ketogluconate and 5 - ketogluconate reductase , reducing 5 - ketogluconate to gluconate , respectively , and that the GntII system is induced by GntH in the presence of idonate or 5 - ketogluconate . RI+GC 14593252 111 Positive Effect of GntR in the Expression of the GntII Genes In addition to the negative effect of GntR , the evidence suggesting the positive regulation by GntR of the GntII genes was obtained by expression analysis in minimum medium containing gluconate ( table 2 ) . RI+GC 14593252 202 Additionally , GntR may also activate the expression of GntII genes when gluconate is present in minimum medium ( table 2 and fig . 4B ) . RI+GC 18346968 259 Expression of the E . coli K - 12 melAB genes , which encode products essential for melibiose metabolism , depends on transcription activation by MelR and CRP , and is triggered by melibiose ( 7,9 ) . RI+GC 10747919 7 Busby § , and Tomofusa Tsuchiya ¶ From the Department of Microbiology , Faculty of Pharmaceutical Sciences , Okayama University , Tsushima , Okayama , 700 – 8530 Japan and the § School of Biosciences , The University of Birmingham , Edgbaston , Birmingham B15 2TT , United Kingdom MelR is an Escherichia coli transcription factor that activates expression of the melAB operon in response to the presence of melibiose in the environment . RI+GC 8010957 12 MelR activity can be triggered by the inclusion of melibiose in the growth medium ; the role of MelR is to activate transcription initiation at the melAB promoter ( pmelAB ) in response to melibiose or , possibly , some other metabolite . RI+GC 16621812 8 Busby * School of Biosciences , University of Birmingham , Edgbaston , Birmingham B15 2TT , United Kingdom Received 29 December 2005 / Accepted 10 February 2006 Transcription of the Escherichia coli melAB operon is regulated by the MelR protein , an AraC family member whose activity is modulated by the binding of melibiose . RI+GC 16621812 15 Supporting evidence for this is provided by the isolation of substitutions in MelR that block melibiose - dependent activation of the melAB promoter while not changing melibiose - independent repression of the melR promoter . RI+GC 16621812 36 It has been proposed ( 30 ) that repression requires the formation of a DNA loop that is stabilized by MelR binding at site R and site 2 and that the presence of melibiose breaks this loop , resulting in derepression of pmelR , occupation of site 2 , and induction of pmelAB ( Fig . 1 ) . RI+GC 16621812 103 Table 3 lists - galactosidase activity measurements , which showed that pmelAB activity is very low in the absence of melibiose and that melibiose triggers a 50 - fold increase in pmelAB activity that is MelR dependent . RI+GC 16621812 136 The simplest explanation of our data is that melibiose switches MelR from a conformation that is unable to activate pmelAB to a conformation that is able to activate pmelAB and that the different MelR substitutions favor adoption of the latter conformation to different extents . RI+GC 16621812 174 In contrast , with four of the mutants ( FL53 , PS81 , TA117 , and ND183 ) , melibiose induces pmelAB activity , but to a lesser level than with wild - type MelR . RI+GC 16621812 200 When triggered by melibiose , wild - type MelR requires the assistance of CRP to activate transcription at pmelAB ( 31 ) . RI+GC 16621812 211 This is because activation requires MelR binding to site 2 that overlaps the pmelAB 35 hexamer element , and melibiose is required for wild - type MelR to occupy this site ( 2 ) . RI+GC 16621812 213 This strong repression is relieved by melibiose and , thus , melibiose toggles MelR between two alternative states , one that activates pmelAB and one that represses pmelR ( Fig . 1B ) . RI+GC 16621812 226 This model is supported by genetic analyses , notably , mutations that alter amino acids in the AraC N - terminal arm that result in AraC - dependent activation of paraBAD in the absence of arabinose ( 19 , 21 , 22 , 34 , 35 ) . RI+GC 10760178 33 Interestingly , AraC - dependent transcription initiation at the araBAD promoter is increased by the cyclic AMP receptor protein ( CRP ) , a well - characterized global regulator , controlled by cyclic AMP ( cAMP ) , that activates the expression of a number of genes in response to a variety of stresses , including glucose starvation ( reviewed by Kolb et al . , 1993 ) . RI+GC 10760178 113 Q 2000 Blackwell Science Ltd , Molecular Microbiology , 36 , 211 ± 222Activation at the E . coli melAB promoter 215 < 1.5 fold increase in the amount of transcript initiating at the melAB promoter in the presence of MelR and melibiose . RI+GC 10760178 120 In the presence of MelR and melibiose , purified RNAP induces clear reactivity of bases around position 210 upstream of the melAB transcript start site ( Fig . 3 , lane h ) . RI+GC 10760178 121 We attribute this MelR - induced hyper - reactivity to open complex formation by RNAP at the melAB promoter , which is clearly dependent on melibiose ( Fig . 3 , compare lanes g and h ) . RI+GC 12675795 8 Summary The Escherichia coli MelR protein is a melibiosetriggered transcription factor , belonging to the AraC family , that activates transcription initiation at the melAB promoter . RI+GC 12675795 40 In previous work , we showed that MelR is a melibioseinduced transcription activator , related to AraC , that is essential for melibiose - induced activation of the E . coli melAB promoter ( Webster et al . , 1989 ) . RI+GC 10760179 7 Summary The Escherichia coli MelR protein is a transcription activator that , in the presence of melibiose , activates expression of the melAB operon by binding to four sites located just upstream of the melAB promoter . RI+GC 10760179 27 AraC is functional as a dimer ; in the presence of arabinose , the conformation of AraC is such that the two subunits of the dimer bind to two adjacent target sites resulting in activation of the araBAD promoter . RI+GC 10760179 35 MelR activity is regulated by melibiose , which is required for activation of transcription initiation at the melAB promoter ( Webster et al . , 1989 ) . RI+GC 10760179 53 We propose that , for optimal repression , MelR forms a loop between Site R and Site 2 , and that this loop is broken in the presence of melibiose when the melAB promoter is activated . RI+GC 10760179 91 Results in Fig . 3 show that , in each case , the single base substitution in the Site R MelR - binding site results in a significant reduction in MelR - dependent repression of the melR promoter in both the absence and presence of melibiose . RI+GC 10760179 127 To investigate this , we constructed a series of KK81 derivatives carrying different mutations in the melAB promoter ( Table 1 ) and measured the consequences of these mutations on MelR - dependent repression of the melR promoter in either the presence of absence of melibiose ( Fig . 5 ) . RI+GC 10760179 149 The presence of melibiose triggers a conformational change in MelR such that the dimer now occupies Site 2 and Site 2 0 and activation of the melAB promoter ensues . RI+GC 11742992 57 Hence , in the absence of MelR , CRP does not activate transcription at the melAB promoter whereas , in the presence of MelR , CRP activates transcription ~ 10 - fold ( Figure 1C ) . RI+GC 8729576 199 In spite of such high similarity , Fnr is associated not with the transport system but with the switching of respiration styles ; i . e . under the anaerobic condition , Fnr activates the transcription of anaerobic enzyme genes , repressing the transcription of oxidase gene ( Spiro & Guest , 1991 ) , together with ArcA , one of the response regulators in Group 1 , that represses the transcription of aerobic respiration enzyme genes ( Iuchi et al . , 1990 ; Iuchi & Lin , 1993 ) . RI+GC 8729576 599 The arcB gene of Escherichia coli encodes a sensor - regulator protein for anaerobic repression of the arc modulon . RI+GC 9484892 119 To confirm that the different levels of expression in the glucose and glycerol media are caused by cAMP / CAP activation , the expression of the manX – lacZ and borG – lacZ fusions was measured in a cya strain ( TP2006 ) . RI+GC 15743943 134 There is no obvious 35 promoter sequence , but a potential CAP site is detectable on the sequence ( Fig . 1A ) , centered at position 61.5 , which is consistent with the strong catabolite repression observed with the nanC fusion . RI+GC 9469834 117 However , cAMP caused a large ( 15 - fold ) stimulation of nagE and a 2.5 - fold stimulation of nagB when the CAP site was located at its functional distance . RI+GC 24593230 45 In the presence of chitobiose / triose , a metabolite of chitobiose , probably monodeacetylated chitobiose - 6P ( Verma and Mahadevan , 2012 ) , causes the ChbR regulatory protein to activate transcription of the chb operon . RI+GC 24593230 104 The NagC repressor inhibits chiP transcription under uninduced conditions through binding to the chiP promoter . RI+GC 24593230 141 However , in both organisms repression of chiP by NagC is inefficient resulting in a relatively high basal level of chiP transcription in the absence of chitobiose ( Figueroa - Bossi et al . , 2009 ) . RI+GC 24593230 151 In the absence of chitosugars ( uninduced ) the chb , chiP and nag operons are repressed by NagC . RI+GC 24593230 184 This suggested that ChiX pairing with the RNA sequence from the chbB - chbC intercistronic spacer – the very mechanism responsible for ChiX inactivation during chitobiose induction – downregulates chbC expression under uninduced conditions . RI+GC 1629153 254 The FNR protein is required for fdnGHI and narGHJI operon expression during anaerobic growth , and the NARL protein is required for induction by nitrate ( 4 ; for a review , see reference 25 ) . RI+GC 2168848 36 We found that expression of the fdnCHI operon was induced anaerobically by nitrate , and required fnr ’ and narL + . RI+GC 11929525 76 As NarL is capable of repressing pnrfA under certain conditions ( Tyson et al . , 1994 ) , the activities of the cloned promoters were determined in the Dlac narL narP + strain , JCB3883 , so nitrite and nitrate activation would be mediated solely by NarP . RI+GC 9696769 126 When wild - type Fnr was expressed from a multicopy plasmid , ( napF - lacZ ) expression was induced approximately sixfold by anaerobiosis ( Table 1 ) . RI+GC 9696769 129 With Fnr ( S73F ) , anaerobic activation of ( napF - lacZ ) expression was significantly reduced ( Table 1 ) . RI+GC 9696769 133 Deletion , mutational , and footprint analyses had indicated that napF operon expression in vivo is induced weakly by either Fnr or NarP alone and strongly by Fnr and NarP together . RI+GC 9696769 172 MBP - NarL antagonizes activation of the napF promoter by Fnr ( D154A ) and MBP - NarP in vitro . RI+GC 9696769 181 DISCUSSION The napF promoter is one of several regulated by Fnr in response to anaerobiosis and by NarL or NarP in response to nitrate and nitrite . RI+GC 17720788 256 However , sequence inspection failed to reveal an apparent Fnr protein binding site in the yeaR - yoaG operon control region ( Fig . 1A ) ( 12 , 40 ) , and microarray analysis revealed Fnr - independent induction of yeaR transcription in response to nitrite ( 12 ) . RI+GC 17720788 287 Recent studies have documented NsrR and Fnr regulation of ytfE ( dnrN ) gene expression patterns similar to those reported here for the yeaR - yoaG operon : NsrR - dependent induction by nitrite and nitric oxide ( or compounds that generate nitric oxide ) and enhanced expression in fnr null strains ( 6 , 20 , 24 ) . RI+GC 18227264 222 Consistent with the hypothesis that YdhY – T has a role in anaerobic metabolism , gel retardation , footprinting , sitedirected mutagenesis and transcript - mapping experiments showed that the oxygen - responsive transcription factor FNR directly activates transcription of ydhY – T under anaerobic conditions by binding at a site located at position 242.5 relative to the transcript start , confirming and extending earlier work that shows that ydhY is expressed from a class II FNR - dependent promoter ( Kang et al . , 2005 ) . RI+GC 18227264 223 Furthermore , ydhY – T expression is regulated by the NarXL and NarPQ nitrate - and nitriteresponsive two - component systems , confirming the results of previous transcription - profiling studies ( Constantinidou et al . , 2006 ) . RI+GC 22101843 27 The twocomponent system CitA / CitB of E . coli is supposed to regulate the expression of the genes for citrate fermentation in response to external citrate under anaerobic conditions ( 20 , 52 ) , similarly to the citrate - responsive two - component system CitA / CitB of Klebsiella pneumoniae ( 6 ) . RI+GC 22101843 123 Thus , the expression of the citCDEFXGT gene cluster of E . coli depends on CitA / CitB , and the system confers induction by citrate in the absence of oxygen and nitrate . RI+GC 22101843 281 Nevertheless , CitA is required for the maximal induction of dcuB - lacZ by citrate ( but not by fumarate ) as shown here and earlier ( 25 ) , and DcuS / DcuR is required for the maximal expression of citC - lacZ . RI+GC 11073923 7 EGAN * Department of Molecular Biosciences , University of Kansas , Lawrence , Kansas 66045 Received 21 August 2000 / Accepted 18 September 2000 The Escherichia coli rhaSR operon encodes two AraC family transcription activators , RhaS and RhaR , and is activated by RhaR in the presence of L - rhamnose . - Galactosidase assays of various rhaS - lacZ promoter fusions combined with mobility shift assays indicated that a cyclic AMP receptor protein ( CRP ) site located at 111.5 is also required for full activation of rhaSR expression . RI+GC 11073923 34 Upon L - rhamnose induction , RhaR was found to activate rhaSR transcription 5 - fold in vitro ( 35 ) ; however , in vivo measurements indicate that overall rhaSR activation was approximately 440 - fold ( 9 ) . RI+GC 11073923 214 This result indicates that in the presence of RhaR , - CTD can contribute to transcription activation at rhaSR , perhaps by interaction with DNA and / or RhaR . RI+GC 1688950 13 Here , we show that purified RhaR can stimulate transcription from the pSr promoter , and that L - rhamnose is required for its activit ’ y . RI+GC 17513476 21 The RhaS protein functions to activate transcription of two of the operons in the Escherichia coli L - rhamnose regulon in response to the availability of L - rhamnose ( 11 , 40 ) . RI+GC 17513476 282 This in vitro transcription system mimics the in vivo activation of rhaBAD by RhaS - CTD and also , to a great extent , the in vivo activation of rhaBAD by full - length RhaS , each in the presence and absence of CRP . RI+GC 9393706 135 However , induction of SoxS synthesis with 50 μm paraquat stimulated transcription of the wild - type mar promoter but not of the marbox promoter mutants 7 or 8 , whether they were in rob + mar or in rob mar strains ( Table 1 ) . RI+GC 12791142 14 We show here that the induction of the AcrAB efflux pump by decanoate and the more lipophilic unconjugated bile salts is mediated by Rob , and that the low - molecularweight inducers specifically bind to the C - terminal , non - DNA - binding domain of Rob . RI+GC 12791142 131 These results leave no doubt that AcrAB induction by fatty acids and lipophilic bile salts is mediated by the Rob protein and occurs with ecologically expected concentrations of these compounds . RI+GC