>Regulatory network in which the protein is involved
>2|P34000|HTH-type transcriptional regulator acrR (Potential acrAB operon repressor)|Escherichia coli O6|TetR
AcrR represses its own expression.
AcrR represses the expression of the acrAB operon.
The expression of micF seems to be under the AcrR control.
MarA, that belongs to AraC/XylS family of activators, upregulates the expression of acrAB.
Consistent with this fact is the presence of an hypothetical MarA binding site upstream of the acrAB operon.
Overexpression of SoxS, upregulates the expression of acrAB.
Transcription of acrAB was increased by general stress conditions (such us 4% ethanol, 0.5M NaCl and stationary phase in Luria-Bertani medium). These conditions increased the transcription of acrR even more strongly than that of acrAB.
Increased transcription of acrAB, caused by general stress conditions, is not mediated by MarA or SoxS.
MarA seems not to be essential for the transcriptional activation of acrAB.
The quorum sensing regulator SdiA also controls the expresión of the AcrAB multidrug efflux pump confering resistance against quinolones.
The acrAB expression is influenced by the growth rate. In slow-growing Escherichia coli cells expression of acrAB is increased, even in the absence of antimicrobial compounds. Up-regulation of acrAB is inversely related to the growth rate of the bacterium.
Glucose limitation increased the level of acrAB expression, at all growth rates, compared with either iron or ammonium limitation. This suggest that cAMP may act, via CRP, as a positive regulator of acrAB expression during carbon limitation.
Transcription of acrAB, upregulated by slow growth, is typical of a gearbox regulated gene and it is interesting to note that the -10 region of the acrAB promoter sequence (-CGAGGTTT-) resembles a gearbox-type sequence homology rather than a sigma-70 consensus sequence.
Slow growth regulation of acrAB is not controlled by RpoS.
>4|P19219|Methylphosphotriester-DNA alkyltransferase|Bacillus subtilis|AraC
In Bacillus subtilis the adaptive response to DNA alkylation is achieved by autologous activation of a divergent regulon composed of the genes for DNA glycosylase (alkA) and two species of DNA alkyltransferase, adaA and adaB.
>5|P06134|ADA regulatory protein (Regulatory protein of adaptative response) [Contains: Methylated-DNA--protein-cysteine methyltransferase (EC 2.1.1.63) (O-6-methylguanine-DNA alkyltransferase)]|Escherichia coli|AraC
Unmethylated Ada protein represses transcription from the ada promoter.
Unmethylated Ada protein activates transcription from the alkA promoter.
The Ada regulon is induced during the stationary phase and protects the cell against active alkylators produced by nitrosation of amino acids in nongrowing cells. This requires the rpoS gene product, which encodes the stationary-phase-specific sigma factor, sigma S, with an important role in stress responses to oxidative damage and osmotic shock.
>7|P26189|ADA regulatory protein (Regulatory protein of adaptative response) [Contains: Methylated-DNA--protein-cysteine methyltransferase (EC 2.1.1.63) (O-6-methylguanine-DNA alkyltransferase)]|Salmonella typhimurium|AraC
The low ability of AdaST to function as a positive regulator could account for the apparent lack of an adaptive response to alkylation damage in S. typhimurium.
>8|P33234|HTH-type transcriptional regulator adiY|Escherichia coli|AraC
The arginine decarboxylase system is maximally induced under conditions of acidic pH, anaerobiosis and rich medium. and AdiY was found to increase the expression of adiA.
>9|Q9ZN78|A-factor receptor protein (A-factor binding protein)|Streptomyces griseus|TetR
There is a consensus to which ArpA binds. ArpA recognizes and binds a 22 bp palyndrome, one half of which is 5’-GG(T/C)CGGT(A/T)(T/C)G(T/G)-3’.
ArpA, in absence of its ligand, A-factor binds to the adpA  promoter region.
ArpA represses the expression of adpA.
AdpA binds a region upstream of the transcriptional start point of strR.
AdpA activates the expression of strR.
StrR activates expression of the streptomycin biosynthesic str/sts gene cluster by binding at least at five of its promoters.
Adp binds at the promoter of adsA and activates its expression.
The adsA product is an extracytoplamic function sigma factor (ECF) that is named sigma-AdsA which is necessary for aerial hyphae formation. Sigma-AdsA is involved only in morphological development and not in secondary metabolic function.
In the model that explains the A-factor dependent regulation cascade inducing streptomycin biosynthesis and morphological development in Streptomyces griseus, ArpA is the ultimate key regulator. In absence of autoinducer, A-factor, ArpA binds the operator sequence at the adpA promoter, repressing adpA expression, avoiding streptomycin biosynthesis and morphological differentiation. When autoinducer, A-factor, is present, it binds to ArpA and the A-factor/ArpA complex dissociates from adpA regulatory region allowing adpA transcription. The transcriptional activator AdpA is a fork in the A-factor dependent regulation cascade. On one hand, AdpA binds the strR promoter region and activates strR expression. StrR switch on expression of the streptomycin biosynthetic str/sts gene cluster, allowing antibiotic biosynthesis. On the other hand, AdpA binds the adsA promoter region and activates adsA expression. The adsA product, the ECF sigma-AdsA, allow morphological development.
>13|P05052|HTH-type transcriptional regulator appY (M5 polypeptide)|Escherichia coli|AraC
AppY is involved in regulation of the cyx appA operon of Escherichia coli by anaerobiosis, phosphate starvation, and growth phase.
The cbd and hya operons exhibit a sigmaS-dependent transient two-fold induction by osmotic upshift.
The cbd operon and the hya operon are highly induced by phosphate starvation depending on AppY. SigmaS concentration is not involved in the phosphate regulation of these operons.
>15|P03021|Arabinose operon regulatory protein|Escherichia coli O157:H7|AraC
In the absence of L-arabinose AraC protein represses expression of the araBAD and araC promoters. With arabinose, AraC activates transcription from the promoters of the catabolic operons. Expression from ParaBAD, ParaE, ParaFGH and ParaC is also regulated by the cyclic AMP-catabolite activator protein.
>25|P17446|HTH-type transcriptional regulator betI|Escherichia coli|TetR
The divergently overlapping betI and betT promoters are regulated in the same manner by three external stimuli: choline, oxygen and osmotic stress.
For cells in aerobic conditions and osmotic stress a partial induction can be observed, but for full expression, the cells also need and external supply of choline.
The regulation of the bet genes by choline, oxygen and osmotic stress is mediated by three separate mechanism: BetI, ArcA and an yet unidentified osmotic signal, respectively.
Choline seems to be an inducer for the expression of betT and betIBA genes, in osmotic stressed cells. When BetI binds choline probably assumes a new conformational state in which is not able to bind the operator.
The regulation by oxygen is mediated by ArcA.
The bet genes belong to the ArcA modulon, consisting of genes repressed by anaerobicity, and the binding of ArcA appears to require a sequence of the betT side of the overlapping promoters.
Fnr is another regulator which controls the activity of many genes which are desrepressed under anaerobic conditions. Fnr is required for full expression of ArcA and in some cases Fnr also directly participates in the regulation of ArcA-controlled genes.
The betIBA genes are cotranscribed from the betI promoter, however, the rate of synthesis of BetI protein, in vivo, constitutes only 10% of that of BetA and BetB dehydrogenase proteins. This fact indicates the existence of a posttranscriptional control of the betIBA operon.
>35|P43506|HTH-type transcriptional repressor Bm3R1|Bacillus megaterium|TetR
In the absence of inducers, Bm3R1 binds two sequences, the bicistronic operator site OIII and the BB3, suppressing the expression of bm3R1 and P450BM-3 genes. In the presence of the inducer, Bm3R1 dissociates from both classes of regulatory sequences and the transcription of P450BM-3 and bm3R1 is elevated to a very high level.
It exists a regulatory loop where exposure to fatty acids as inducers, removes Bm3R1 from the DNA regulatory sequences, resulting in the induction of P450BM-3, then the inductor fatty acid is metabolised and no longer binds to Bm3R1, which results in the switch-off of P450BM-3 transcription.
It seems that Bm3R1 is implicated in the regulation of P450BM-1.
Bm3R1 binds three regions with regard to P450BM-1, OI, OII and BB1.
However the binding of Bm3R1 to these three regulatory sequences is not directly inhibited in vitro by barbiturates.
It seems that Bm3R1 represses the expression of bm1P1.
The bm1P1 gene encodes a TetR repressors family.
The bm1p1 gene located immediately upstream of the P450BM-1 gene, and its product appears to be implicated in the control of the expression of P450BM-1. An hypothetical mechanism that involves to Bm3R1 as repressor and Bm1P1 as activator: Bm3R1 could interfer with the binding of Bm1p1 to the regulatory regions of P450BM-1.
This hypothetical mechanism for regulation of the P450BM-1 transcription, exposes that in absence of inducers, Bm3R1 exits in a conformation that binds the operator and Barbie box sites doing enhaces DNA loop formation in the 5'-flanking region of the P450BM-1 gene by protein-protein interaction between the Bm3R1 molecules. As consequence, the P450BM-1 gene promoter are not accesible and transcription of P450BM-1 gene is inhibited. In presence of inducers (barbiturates), Bm3R1 assumes another alosteric form that can still bind OI and OII and Barbie box elements. However, under the influence of Bm1P1 the Bm3R1-inducer complexes dissociate from OI and OII and Barbie box sequences and DNA looping is reversed, promoter are accessible and P450BM-1 gene can be expressed.
However there are evidences against Bm1P1 as a positive transcription factor involved in barbiturate-mediated induction of P450BM-1 and evidences against the Barbie box, BB1, as a key element responsible for induction of P450BM-1 by barbiturates.
It is not detected binding of Bm1P1 to the 5’ flanking region, including the Barbie box, of the P450BM-1 gene.
Induction of P450BM-1 by pentobarbital is unlike to be mediated by bm1P1.
It seems that the Barbie box is not the key element responsible for barbiturate-mediated induction of P450BM-1. The sequence within the Barbie box is important for negative regulation of P450BM-1 gene expression in the absence of pentobarbital.
Bm3R1 may regulate P450BM-1 gene expression in an indirect manner rather than by direct binding to the 5’ flanking region of the P450BM-1 gene.
>38|P25393|CFA/I fimbrial subunit D (Colonization factor antigen I subunit D)|Escherichia coli|AraC
CfaD removes the repressive effect mediated by H-NS.
>44|Q9ZFU7|HTH-type transcriptional regulator eutR (Ethanolamine operon regulatory protein)|Salmonella typhimurium|AraC
The PI promoter is activated by EutR when both ethanolamine and AdoB12 are present and requires CRP protein as a global regulator.
>47|Q47129|Transcriptional activator feaR|Escherichia coli|AraC
It seems possible that tyramine and the MaoB protein activate the transcription of maoA by binding to the regulatory region upstream of the maoA gene.
>60|P41782|Transcriptional regulator hilD|Salmonella typhimurium|AraC
The HilA gene expression is regulated by genetic elements encoded on SPI-1 (hilC/sirC/sprA and hilD), as well as by elements which reside outside the SPI-1 (phoP/phoQ and sirA). HilA is tightly regulated in response to many environmental conditions, including oxygen, osmolarity and pH.
>64|P39437|Invasion protein invF|Salmonella typhimurium|AraC
The expression of sigDE, which is not linked to SPI1, is co-ordinately regulated with the SPI1 genes and is dependent on the SirA, HilA and InvF transcriptional regulators Expression of the sip/ssp genes is partly regulated in from the Hil-A dependent promoter, plus an invF-dependent promoter.
>69|O33813|Lactose operon transcription activator|Staphylococcus xylosus|AraC
The lacPH promoter is also subject to carbon catabolite repression mediated by the catabolite control protein CcpA. When glucose is present in the growth medium, lacPH transcription is reduced.
>72|P21308|HTH-type transcriptional regulator luxR|Vibrio harveyi|TetR
LuxR represses its own expression by binding to two sites within its own promoter.
The direct role of LuxR on the regulation of the operon luxCDABEGH remains unknown.
The luciferase operon in Vibrio harveyi is under the control of a two signal-response quorum sensing system with at least seven proteins implicated: LuxLM, LuxS, LuxN, LuxQ, LuxT, LucU and LuxO. LuxLM synthetizes one autoinducer, N-(3-hydroxybutanoyl)-homoserine lactone (AI-1). LuxS synthetizes chemically undefined autoinducer (AI-2). The sensor proteins LuxN and LuxQ interact with autoinducers, AI-1 and AI-2, respectively. Signalling from both sensors, that function as kinases, converges at LuxU, a shared phosphorelay protein. Finally, LuxU transfer a signal to the response regulator protein LuxO [whose expression is regulated by LuxT, a repressor which shares homology with the TetR/AcrR family, with a footprint binding between 117 and 149 bp upstream from the luxO initiation codon.
Phospho-LuxO is responsible of the expression of the luciferase structural operon, luxCDABEGH, at low cell densities and low autoinducer concentrations. As the cell density increases, the autoinducers accumulate in the culture medium and LuxN and luxQ act as phosphatase and dephosphorylate LuxO which results in the induction of the lux operon.
CRP (camp receptor protein) also bind to the promoter of the luxR gene and the luxCDABEGH CRP and MetR.
CRP acts as an activator of the luminescence.
MetR acts as a repressor of luminescence.
>82|P39897|HTH-type transcriptional regulator mtrR|Neisseria gonorrhoeae|TetR
Gonococci can modulate their resistance to hydrophobic antimicrobial agents (Has) through both positive and negative transcriptional control of the mtrCDE gene expression.
The protein responsible for the negative control is the MtrR repressor that represses the expression of the mtrR and mtrCDE genes.
MtrA is involved in an inducible positive control of the mtrCDE gene expression. MtrA belongs to AraC/XylS family of transcriptional activators.
It is not known whether MtrA activates directly or indirectly transcription of the mtrCDE operon.
Gonococci can express constitutive resistance to hydrophobic antimicrobial agents by mutation in the mtrR coding region or in its promoter region, that reduces or abrogates the MtrR repression of mtrCDE genes.
MtrR might act directly or indirectly as a positive regulator of farAB gene expression.
>90|P72171|Ornithine utilization regulator|Pseudomonas aeruginosa|AraC
OAcT expression is repressed in the presence of citrate. Expression of OAcT is maximally enhanced by the presence of ornithine in the growth medium and considerably depressed by the presence of glutamate.
>93|P40883|Regulatory protein pchR|Pseudomonas aeruginosa|AraC
The activation of fptA by PchR depends directly on pyochelin. It appears that PchR functions in activation when pyochelin is present and in repression when it is absent.
>97|Q05587|Regulatory protein pocR|Salmonella typhimurium|AraC
Expression of the pdu and cob operons is induced by propanediol and globally controlled by the ArcA and CRP systems.
Chen et al. proposed the following model for control of the pdu/cob regulon: -OFF state: during aerobic growth in glucose with propanediol. All the promoters are inactive except for Ppoc that exhibits a basal activity; -STANDBY state: Without propanediol and with a poor carbon source or under anaerobic conditions. The P1 promoter is activated by IHF with FNR or CRP proteins acting alternatively at their nearby binding sites. This binding occludes the pdu promoter. CRP also stimulates Ppoc. PduF and PocR function preparing cells to take up and to respond to propanediol; -ON state: with propanediol. Propanediol enters and interacts at the cytosol with PocR stimulating P1 and P2 promoters. ArcA stimulates the P2 promoter and CRP stimulates Ppoc promoter. Finally, the pdu and cob operons are induced.
>100|P23217|HTH-type transcriptional regulator qacR|Staphylococcus aureus subsp. aureus Mu50|TetR
QacR does not autoregulates its own expression.
QacR is a trans-acting repressor of qacA.
Binding of QacR to DNA requires a 6 bp long spacer region between the two IR1 hal-sites.
In absence of inducers QacR is bound to its DNA operator sequence, IR1, repressing expression of the qacA gene. When inducers are present, QacR interacts directly with them being released from its operator site. This lack of repression results in an increase of the transcription of the qacA gene.
>108|P09378|L-rhamnose operon transcriptional activator rhaR|Escherichia coli|AraC
The rhaSR operon is activated by RhaR in the presence of L-rhamnose. Cyclic AMP receptor protein (CRP) is also required for full activation of the rhaSR expression.
>110|P09377|L-rhamnose operon regulatory protein rhaS|Escherichia coli|AraC
L-rhamnose induction of rhaBAD expression first requires the induction of rhaSR expression which leads to the accumulation of RhaS, and finally activation of RhaBAD expression.
Cyclic AMP receptor protein (CRP) participates in the activation of the RhaBAD operon.
RhaS alone is able to activate rhaBAD expression by about 1,000-fold. In the presence of RhaS, CRP activates rhaBAD an additional 30- to 50-fold; however, CRP is unable to activate to a significant extent in the absence of RhaS.
>122|P39885|HTH-type transcriptional regulator tcmR (Tetracenomycin C transcriptional repressor)|Streptomyces glaucescens|TetR
In absence of tetracenomycin C, TcmR binds to the two operator sequences situated in the tcmA-tcmR intergenic region, blocking the tcmA and tcmR-p1 promoters. Thus TcmR represses the tcmA and its own expression.
TcmR does not bind the tcmR-p2 promoter region. This fact is consistent with the description of p2 as a constitutive promoter for the tcmR gene.
The antibiotic tetracenomycin C interacts with TcmR repressor protein reducing its DNA-binding ability and thus, both genes, tcmA and tcmR, are expressed.
A plausible model for regulation of tcmA-tcmR genes and tetracenomycin C resistance: Initially, constitutive, low levels synthesis of tcmR mRNA from the tcmR-p2 promoter generates a sufficient amount of TcmR protein to repress tcmR and tcmA transcription by binding to the operator sites upstream of those genes. As the TcmR concentration in the cell reaches a point where repressor-binding sites are completely occupied, less transcription from the tcmR-p2 promoter could be expected. Eventually, expression of tcm biosynthetic genes results in production of tetracenomycin C, which binds to the TcmR repressor and thereby prevents the repressor from binding to its operator sites. This allows expression of the tcmA gene, resulting in tetracenomycin C export and resistance as well as a higher level of tcmR expression, but now, from the tcmR-p1 promoter. This results in high amounts of TcmR and once the concentration of antibiotic in the cell drops, because of its export by TcmA, TcmR binds its operator sites and shutoffs the expression of both genes, going back to the initial situation.
>124|P03038|Tetracycline repressor protein class A from transposon 1721|Escherichia coli|TetR
TetR, in absence of inducer, has a DNA-binding conformation, binding to the two tet operators and resulting in repression of the transcription of tetR and tetA. In presence of inducer, TetR adopts a non-DNA binding conformation separating from the operators and starting the expression of both genes.
>126|P04483|Tetracycline repressor protein class B from transposon Tn10|Escherichia coli|TetR
TetR, in absence of inducer, has a DNA-binding conformation, binding to the two tet operators and resulting in repression of the transcription of tetR and tetA. In presence of inducer, TetR adopts a non-DNA binding conformation separating from the operators and   starting the expression of both genes.
The tet genes are differentially regulated so that TetR synthesis can occurs before the tetA is expressed.
tetA is regulated by TetR bound to either tetO1 or tetO2.
Expression of tetR is only marginally reduced when TetR is bound to tetO2 and occupation of tetO1 with TetR turns off completely transcription from the promoter of tetR.
The recognition helix of TetR interacts in different fashions with the tetO1 and tetO2 operators.
>127|P03039|Tetracycline repressor protein class C|Escherichia coli|TetR
TetR, in absence of inducer, has a DNA-binding conformation, binding to the two tet operators and resulting in repression of the transcription of tetR and tetA. In presence of inducer, TetR adopts a non-DNA binding conformation separating from the operators and starting the expression of both genes.
>128|P09164|Tetracycline repressor protein class D|Escherichia coli|TetR
TetR, in absence of inducer, has a DNA-binding conformation, binding to the two tet operators and resulting in repression of the transcription of tetR and tetA. In presence of inducer, TetR adopts a non-DNA binding conformation separating from the operators and starting the expression of both genes.
The recognition helix of TetR interacts in different fashions with the tetO1 and tetO2 operators.
>138|P43462|Probable thc operon regulatory protein|Rhodococcus erythropolis|AraC
Cysteine represses the expression the expression of the thcB gene.
>145|P32326|Urease operon transcriptional activator|Escherichia coli|AraC
Urea-dependent expression requires UreR.
>151|Q04248|Virulence regulon transcriptional activator virF|Shigella dysenteriae|AraC
The activation of VirB by VirF is antagonized at 30ºC by HN-S.
>167|Q04710|XylDLEGF operon transcriptional activator 1|Pseudomonas putida|AraC
In cells growing in the presence of aromatic hydrocarbons (i.e. toluene and m-xylene) it appears that expression of both meta-1 and meta-2 pathways is achieved via a cascade regulatory system in which the ultimate regulator is the effector-activated XylR protein.
>170|Q05335|XYLDLEGF operon transcriptional activator 3|Pseudomonas putida|AraC
The XylS3 regulatory protein activates transcription of meta-1 and meta-2 operons.
>245|O24739|BarB|Streptomyces virginiae|TetR
BarA represses transcription of the barB gene in absence of the VB autoinducer.
The expression of barB happens just before the production of virginiamycin.
It seems that the VB autoinducer and its receptor BarA regulate the expression of barB, which in turn control virginiamycin production.
>248|O30343|Hemagglutinin/protease regulatory protein|Vibrio cholerae|TetR
The expression of hapR is under the control of a quorum sensing system that implies the LuxS, LuxPQ and LuxO proteins. LuxS controls the synthesis of the autoinducer, a borate diester (AI-2 from Vibrio harveyi). LuxPQ is the receptor for the autoinducer and LuxO is the response regulator that controls the expression of hapR. At low cell densities, hapR is repressed by LuxO, but at high cell densities, LuxO fails to repress the expression of hapR.
HapR represses the expression of the virulence cascade.
A critical regulatory step in the cascade is activation of tcpPH expression by AphA and AphB transcriptional activators. HapR directly repress aphA expression by binding to the aphA regulatory region, which in turn results in the lack of expression of tcpPH.
The repression of tcpPH blocks the expression of toxT.
ToxT is a transcriptional activator, belonging to the AraC/XylS family, that activates the expression of the virulence genes (tcpPH, tcpA-F, acf genes, ctxA and ctxB).
In this way, at high cell density, HapR directly represses the virulence cascade in Vibrio cholerae.
HapR is absolutely required for hapA expression in Vibrio cholerae.
The gene hapA encodes a secreted soluble haemagglutinin with zinc metalloprotease activity, called HA protease.
HapR seems to regulate also the expression of secreted proteases other than the HA protease.
HapR represses the biofilm formation.
One speculative model proposes that on initial (low bacterial cell density) colonization of a host by Vibrio cholerae, LuxO represses hapR expression and allows the expression of aphA and then the expression of tcpP. This, in turn, results in the expression of the virulence factors in ToxR regulon. These virulence factors enable Vibrio cholerae to colonize the small intestine, multiply, and produce cholera toxin. When a high cell density is reached, autoinducer accumulates, and LuxO no longer represses hapR expression. Subsequent production of HapR, represses aphA and in turn tcpP and ToxR regulon expression. In contrast, at high cell density, HapR activates expression of hapA, which encodes the HA protease. Protease expression might promote detachment of Vibrio cholerae cells, and thus facilitate establishment of new infection foci elsewhere within the gastrointestinal tract, or alternatively, promote the exit of Vibrio cholerae from the host.
>253|O33453|CymR|Pseudomonas putida|TetR
CymR is the regulatory protein, that in the absence of the inducer, represses expression of both the cym and the cmt adjacent operons.
>258|O52834|AlcR (Alcaligin siderophore system regulator)|Bordetella bronchiseptica|AraC
Alcaligin biosynthesis requires the action of an ornithine decarboxylase encoded by the odc gene and the alcABC gene products.
Fur represses alcaligin biosynthesis. Fur is a ferric uptake regulatory protein which acts as a corepressor with ferrous iron under conditions of iron abundance.
>259|O52846|XylS/AraC transcriptional regulator|Bacillus megaterium|AraC
Absence of glucose leads to weak transcription of bgaM but clear transcription of the bgaR operon. When lactose is added exclusively, it acts as an effector of BgaR, resulting in transcriptional activation of bgaM.
>262|O68276|Putative DNA-binding protein Bm1P1|Bacillus megaterium|TetR
bm1P1 negatively affects the basal-level of expression of P450BM-1.
bm1P1 is under negative regulation by Bm3R1.
The way in which Bm1P1 affects expression of P450BM-1 remains unclear.
Bm3R1 regulates P450BM-1 gene expression in an indirect manner.
The bm1P1 3’ flanking region inhibits Bm1P1 production.
The inhibition of the bm1P1 3’ flanking region over Bm1P1 production occurs in an orientation-independent manner.
The bm1P1 3’ flanking region acts only in cis.
The effect of the bm1P1 3’ flanking region on Bm1P1 production is independent of the bm1P1 promoter region.
There is a Barbie box element within the start of the bm1P1 coding region [(+98)ATAAAAAGCTGGTGC(+84)].
Barbie box elements are a type of DNA sequences 15-17 bp long, situated at the 5’ regulatory regions of all, eukaryotic and prokaryotic genes that encode barbiturate-inducible proteins.
Bm3R1 binds to this Barbie box element.
The Barbie box does not seem to be a key element in barbiturate mediated  induction of P450BM-1.
>263|O68442|Regulatory protein|Agrobacterium tumefaciens|TetR
The isoflavonoid coumestrol induces ifeA expression.
>269|O70020|IcaR|Staphylococcus epidermidis|TetR
IcaR represses the expression of the ica operon.
It seems that IcaR does not regulate its own expression.
The 30% of biofilm-negative mutants in S. epidermidis constain the insertion element IS256 at a specific hotspot within icaA or icaC. This transposition is reversible.
IcaR is a repressor of the ica operon, but IcaR activity alone does not completely repress ica operon expression.
Activation of the ica operon by ethanol is icaR dependent.
The induction of ica operon expression by NaCl-glucose is small but significant. This induction is icaR independent and is rsbU/sigB dependent.
Staphylococcus epidermidis Tü3298 contains the sigB operon.
icaR transcription displayed a 5.6-fold decrease in the presence of ethanol but was not affected by ClNa-glucose. Given that the icaR gene does not appear to regulate its own expression, ethanol repression of icaR may involve an additional transcription factor.
Anaerobic conditions induce expression of ica operon.
>291|Q8KLP4|Repressor|Stenotrophomonas maltophilia|TetR
SmeT represses its own expression.
>328|Q8VQC6|VanT|Listonella anguillarum|TetR
VanT positively regulates expression of the metalloprotease gene empA.
VanT regulates, activating, expression of vps73, serA and hpdA genes.
VanT acts a positive regulator of the genes sat-vps73, which are involved in biofilm formation.
>387|Q46985|Regulator of the 4HPA-hydroxylase operon|Escherichia coli|AraC
HpaX encodes a functional 4-HPA transporter that facilitates the activation of the pbc promoter when very low concentrations of 4-HPA  are present in the culture medium.
>393|Q51597|Cam repressor|Pseudomonas putida|TetR
CamR represses its own expression.
Expression of the camDCAB operon and the divergently oriented camR gene is negatively regulated through interaction of the CamR protein with the single operator located in the overlapping promoter region between the camDCAB operon and the camR gene. In the presence of D-camphor these genes are divergently transcribed from the overlapping promoters.
>405|Q56153|JadR2|Streptomyces venezuelae|TetR
Jadomycin B is formed when cultures grown in a medium containing poorly assimalated sources of carbon and nitrogen are exposed to additional stress, such as heat shock, phage infection, or exposure to toxic concentrations of ethanol.
jadR1 is required as positive regulator for expression of jadomycin biosynthesis genes but does not mediate the stress response.
jadR2 mediates a repression that was postulated to decrease expression of the genes for jadomycin biosynthesis by countering activation by the positive regulator encoded by jadR1.
jadR1 and jadR2 form and interacting stress-responsive regulatory system for jadomycin B production.
>416|Q60011|Virginiae butanolide receptor|Streptomyces virginiae|TetR
BarA autoregulates its own transcription.
BarA represses the transcription of the gene barB.
BarA represses expression of the repressor BarB untill the concentration of VB autoinducer reaches the threshold value, then BarB may be expressed alowing virginiamycin production.
>841|Q9AIU0|Regulatory protein TtgR|Pseudomonas putida|TetR
A regulator may be involved in the control of the TtgR expression.
A leucine-responsive regulatory protein-like named TtgX seems to repress the expression of the ttgR gene in absence of toluene.
It is unknown whether the effect of TtgX on expression of ttgR is directly or indirectly.
In absence of inducers, TtgR is bound to its operator sequence repressing the expression of both, ttgR and ttgABC genes. When the inducers are present, they bind   to TtgR being released from its operator site. This lack of repression results in an increase of the transcription of both, ttgR and ttgABC genes.
The TtgABC pump is expressed at high basal levels.
>844|Q9AJL5|VarR|Streptomyces virginiae|TetR
The transcription of the varS-varR operon is induced by the addition of virginiamycin S (VS) after 8 h of culture, but not by virginiamycin M1.
VB-BarA system does not directly control varS-varR transcription.
VarR seems to repress the transcription of the varS-varR operon by binding to the varS promoter region until the onset of virginiamycin S production. When virginiomycin S production starts, the repression is relieved though the dissociation of VarR from the promoter region of varS.
A possible model for the transcriptional regulation of the varS-varR operon can be deduced as follows: before the onset of the butyrolactone autoregulators VB (virginiae butanolides), and before viginiamycin S production, transcription of varS-varR is likely to be repressed by a small but sufficient amount of VarR derived from the basal level transcription of varR. Alternatively, vegetative sigma factors might not work for transcription from the varS promoter. When VB production starts, VB-bound BarA dissociates from the barB promoter and induces bicistronic barB-varS transcription, which confers VS resistance before the onset of virginiamycin production (that requires expression of the barB gene). When production of virginiamycin starts, the binding of VS to VarR causes VarR to dissociate from the varS promoter region thereby leading to the derepression of varS-varR transcription.
>852|Q9ANS7|LuxT|Vibrio harveyi|TetR
LuxT is a repressor of the luxO expression.
The luciferase operon in Vibrio harveyi is under the control of a two signal-response quorum sensing system with at least seven proteins implicated: LuxLM, LuxS, LuxN, LuxQ, LuxT, LuxU and LuxO. LuxLM synthetizes one autoinducer, N-(3-hydroxybutanoyl)-homoserine lactone (AI-1). LuxS synthetizes chemically undefined autoinducer (AI-2). The sensor proteins LuxN and LuxQ interact with autoinducers, AI-1 and AI-2, respectively. Signalling from both sensors, that function as kinases, converges at LuxU, a shared phosphorelay protein. Finally, LuxU transfer a signal to the response regulator protein LuxO. Phospho-LuxO is responsible of the expression of the luciferase structural operon, luxCDABEGH.
LuxT appears to be a general rather than lux-specific regulator.
>862|Q9EVJ6|Repressor protein MphR(A)|Escherichia coli|TetR
MphR(A) represses its own expression by repressing the transcription of the mph(A)-mrx-mphR(A) operon.
The transcription of the mph(A)-mrx-mphR(A) operon is repressed by the binding of MphR(A) to the promoter of the mph(A) gene and is activated upon inhibition of binding of MphR(A) to the promoter in the presence of erythromycin.
>866|Q9F0Y2|Pip|Streptomyces coelicolor|TetR
Pristinamycin I induces the expression of the pep gene which product, Pep, confers resistance against this antibiotic.
>879|Q9F6W0|CasR|Rhizobium etli|TetR
The gene casA is exclusively expressed during colonization and infection of Rhizobium etli with the host.
casA regulation occurs independently of known regulatory mechanisms of nodulation and nitrogen fixation genes.
>923|Q9L8G8|SmcR (VvpR)|Vibrio vulnificus|TetR
It is likely that the regulatory role of ScmR involves extracellular factors (autoinducers).
There is a Vibrio vulnificus, ToxRS homolog (ToxRSVv) to ToxRS of the Vibrio cholerae (ToxRSVc), and both systems show functional homology.
The ToxRSVv regulates the production of hemolysin, the most potent exotoxin produced by this organism.
This fact raises possible similarity of the different regulatory mechanisms of virulence between Vibrio vulnificus and Vibrio cholerae. We speculate that SmcR similarly to HapR could be repressing a hypothetical aphA homolog in Vibrio vulnificus. This could explain why a transcriptional repressor can act also as an activator of several virulence factors.
ToxRS, in Vibrio cholerae, exerts its action together TcpPH, whose expression is under the control of the AphA transcriptional activator.
ScmR appears to be part of a quorum-sensing system similarly to LuxR from Vibrio harveyi or HapR from Vibrio cholerae.
>963|Q9R9T9|Efflux pump regulator SrpR|Pseudomonas putida|TetR
The srpR and srpS products are involved in the regulation of srpABC efflux pump.
The regulatory mechanisms of the srp operon have not yet been clarified and the role of the two putative regulators, srpR and srpS, remains unclear.
Flagella biosynthetic insertion mutants have been isolated showing  downregulation of the srp locus.
>966|Q9RAJ1|Inactive regulatory protein|Mycobacterium sp. GP1|TetR
In Mycobacterium sp. strain GP1 the product of the gene dhaR is inactive leading to constitutive expression of the gene dhaA.
>983|Q9RPK9|TarA|Streptomyces tendae|TetR
TarA negatively regulates its own synthesis.
>995|Q9WW32|MtrA|Neisseria gonorrhoeae|AraC
MtrA is an activator of the transcription of the mtr gene cluster.
>1011|Q9XCC5|Hypothetical transcriptional regulator TylQ|Streptomyces fradiae|TetR
TylP represses the tylQ promoter.
TylQ represses (directly or indirectly) the expression of the activator tylR.
For studies of regulation of tylosin biosynthesis were used Streptmyces fradiae mycelium after grown for 18 hr and 40 hr (before and after the onset of tylosin production). The regulatory network begins with tylR which expression is activated at 40 hr. Before, the absence of TylP allows expression of TylQ repressing expression of the transcritional activator TylR, that maintains repressed expression of genes for tylosin biosynthesis. At later times (40 hr), TylP is expressed, repressing the expression of TylQ and alowing the expression of the transcriptional activator TylR, which triggers tylosin biosynthesis.
>1012|Q9XCC7|Gamma-butyrolactone receptor protein TylP|Streptomyces fradiae|TetR
The tyl cluster contains at least five regulatory genes, tylR, tylS, tylT, tylP and tylQ.
TylP represses its own repressor.
TylP represses the tylQ promoter.
TylP is not the only regulator of tylQ.
The expression of tylS might be controled by TylP.
TylP negatively influeces expression of tlrD, tylMIII and tylO.
The effect of TylP is not confined to tylosin production pathway and affects to morfological deferentiation.
For studies of regulation of tylosin biosynthesis were used Streptmyces fradiae mycelium after grown for 18 hr and 40 hr (before and after the onset of tylosin production). The regulatory network begins with tylR which expression is activated at 40 hr. Before, the absence of TylP allows expression of TylQ repressing expression of the transcritional activator TylR, that maintains repressed expression of genes for tylosin biosynthesis. At later times (40 hr), TylP is expressed, repressing the expression of TylQ and alowing the expression of the transcriptional activator TylR, which triggers tylosin biosynthesis.
>1025|Q9Z676|Regulatory protein GdhBR|Pantoea citrea|AraC
gdhB is constitutively expressed during the exponential growth phase and is induced in the stationary phase probably by gdhBR.
>1033|Q9ZGB7|LanK|Streptomyces cyanogenus|TetR
A hypothetical regulatory model suggest that LanK is a regulator of landomycin A resistance and functions by repressing the expression of its adjacent and divergently-oriented gene, lanJ.
lanI is situated 2 kb upstream from lanE. lanI is similar to the positive regulator jadR1 from Streptomyces venezuelae.
Like JadR1, LanI can be classified as representative of the OmpR-PhoB subfamily of regulator proteins.
LanI acts as a positive regulator in landomycin biosynthesis.
In Streptomyces venezuelae it seems that JadR2, equivalent to LanK, represses the expression of jadR1 which is equivalent to lanI.
LanK could repress the expression of lanI.
>1369|O31249|Transcriptional regulator of XylS /AraC family (XylS/AraC family)|Acinetobacter sp. ADP1|AraC
Transcription of alkM depends strictly on AlkR and is inducible by hydrocarbons of different chain lengths. It seems to be repressed by oxidized alkane derivatives, while alkR is transcribed at a low level.
Limitations in inducibility in the stationary phase indicate an influence of general starvation or some form of catabolite repression.
>1383|O50285|OpaR|Vibrio parahaemolyticus|TetR
Vibrio parahaemolyticus undergoes phase variation between opaque and translucent colony morphologies.
Opaque-translucent variation involves genomic rearrangements that affect to the gene opaR.
opaR is not expressed in translucent strains due to inactivation of the gene by an insertion sequence.
opaR is expressed in opaque strains because the gene remains intact.
It is not clear whether environmental conditions influence opaque-translucent switching in Vibrio parahaemolyticus or whether this variation is random.
The gene products that are responsible for Vibrio parahaemolyticus opaque-translucent phenotypes, and that presumably are regulated by OpaR, have not been identified.
Vibrio parahaemolyticus contains a toxRS operon higly similar to toxRS from Vibrio cholerae.
This fact raises the possibility of a regulatory model for opaR similar to hapR one.
>1386|O52066|AlcR (Transcriptional regulator)|Bordetella pertussis|AraC
Alcaligin biosynthesis requires the action of an ornithine decarboxylase encoded by the odc gene and the alcABC gene products.
Fur represses alcaligin biosynthesis. Fur is a ferric uptake regulatory protein which acts as a corepressor with ferrous iron under conditions of iron abundance.
>1431|O86852|Gamma-butyrolactone binding protein|Streptomyces coelicolor|TetR
ScbR negatively regulates its own transcription, and the relief of this repression requires SCB1 produced via scbA expression.
ScbR is necessary for expression of scbA.
It seems that ScbA activates its own transcription.
ScbR negatively regulates the transcription of scbA, but it seems that is necessary the presence of scbA for its own expression, and this fact does not simply reflect the loss of SCB1 synthesis.
Transcription of scbA and scbR occurs in a growth phase-dependent manner.
The divergent transcripts of scbA and scbR overlap by 53 bp. It is thus conceivable that RNA polymerase molecules transcribing from one promoter could impede transcription initiation and/or extension from the other.
The system ScbR/SCB1 controls the production of actinorhodin and undecylprodigiosin, the two pigmented antibitics made by Streptomyces coelicolor.
ScbR regulate biosynthesis of actinorhodin and undecylprodigiosin, in a indirectly way.
The regulatory protein AsfB acts as an activator of the SCB1 production.
The asf mutation reduces transcription of the regulatory genes actII-ORF4 and redD, that control the biosynthesis of actinorhodin and undecylprodigiosin respectively.
A tentative working model for the regulation of gamma-butyrolactone and antibiotic production in Streptomyces coelicolor is as follows: During exponential growth, the low basal level of scbR transcription provides sufficient ligand-free ScbR to largely repress transcription its own gene, and possibly that of scbA, by binding sites R and A respectively. Under these conditions, insufficient ScbR is made to repress synthesis of an unidentified negative regulator of antibiotic production. Any ScbA resulting from the low basal level of scbA transcription that is presumed to occur under these conditions would be insufficient to bring about perceptible SCB1 production. During transition phase, ScbA accumulates to a level where sufficient ScbR-ScbA complexes can be formed for activation of scbA transcription, leading to a burst of SCB1 production. The resulting SCB1 then binds th ScbR, preventing ScbR from binding at site R, relieving self-expression, but also inactivating the ScbR-ScbA complex, thus reducing scbA transcription. The consequent fall in SCB1 levels, coupled with remaining high levels of ScbR, leads to repression of the repressor(/s) of the antibiotic production.
>2160|Q53901|ActII protein (Putative transcriptional regulatory protein)|Streptomyces coelicolor|TetR
actII-1 represses the expression of the actII-2 actII-3 operon.
The actII-2/3 promoter is strongly repressed by the actII-1 gene product.
The actII-1 gene product also represses its own synthesis.
Both promoters are most active during actinorhodin production.
>2162|Q56951|AraC-like regulator YbtA (Transcriptional regulator YbtA)|Yersinia pestis|AraC
Synthesis of Psn is positively regulated by iron and probably by the presence of its cognate siderophore. The Fur protein inhibits Psn synthesis.
>4196|Q9F8V9|TetR family bacterial regulatory protein|Agrobacterium tumefaciens|TetR
The 348 bp DNA sequence upstream of ameR does not have promoter activity.
It appears that ameR forms an operon with the upstream gene(s) and probably ameR is subject to the same kind of regulation as the purC gene.
>4308|Q9JN89|Hypothetical protein mmfR (Putative lactone-dependent transcriptional regulator (TetR-family), MmfR)|Streptomyces coelicolor|TetR
A putative gamma-butyrolactone synthetized by the MmfL protein may be the ligand recognized by the MmfR regulatory protein, controlling the expression of the mmfR and mmfL genes.
>4834|16131152|putative transcriptional regulator|Escherichia coli K12|TetR
The acrEF operon is expressed only weakly in Escherichia coli.
It is likely that expression of the acrEF operon is not essential for Escherichia coli  cells, in which the acrAB operon is expressed, to survive in a milieu containig harmful compounds. The acrEF operon might be part of a strategy which allows Escherichia coli to survive under harmful conditions in the event that the acrAB genes become inactive.
>4926|16077337|transcriptional regulator|Bacillus subtilis subsp. subtilis str. 168|TetR
LmrA represses expression of the operon lmrAB.
>5056|15597216|probable transcriptional regulator|Pseudomonas aeruginosa PAO1|TetR
It seems that the functional regulation of the amrAB pump is quite complex and it must exit other regulatory system besides the amrR gene.
>5116|15600252|probable transcriptional regulator|Pseudomonas aeruginosa PAO1|TetR
Until now not much was known about specific regulatory proteins involved in pha genes expression.
The ntrB and ntrC genes involved in nitrogen regulation in various bacteria are also involved in the regulation of poly-3-hydroxybutyrate synthesis by ammonia in Azospirillum brasilense SP7.
PhabRPs is a transcriptional activator belonging to the AraC-XylS family involved in the expression of the genes required for the synthesis of the poly-3-hydroxibutyrate homopolymer.
PhaS from Pseudomonas putida KT2440 is a putative regulatory protein that shows similarity to the sensor component of the two-component regulatory systems and  contains a histidine protein kinase and response regulator domain.
GacS is a transmembrane sensor kinase homolog that regulates the alginate and poly-3-hydroxibutyrate polymer production in Actobacter vinelandii.
PHA accumulation from gluconate in Pseudomonas aeruginosa PAO1 requires a functional RpoN sigma factor.
PhaF of Pseudomonas oleovorans is involved in the transcriptional regulation of pha genes expression and has a structural function binding to PHA granules.
Another member of the TetR family that controls the synthesis of PHA (specifically poly-3-hydroxibutyrate) is LuxR from Vibrio harveyi (besides to control bioluminascence).
>5460|15928251|ica operon transcriptional regulator IcaR|Staphylococcus aureus subsp. aureus N315|TetR
IcaR is a repressor of the production of PNAG (polysaccharide N-acetyl glucosamine).
It seems that other regulators participate in the regulation of the ica operon.
Several known stimuli induce PNAG production in vitro including elevated glucose, high osmolarity, low levels of ethanol, iron restriction and oxygen depravation. These stimuli may work in part through the alternative sigma factor, sigma-B. These findings, along with reports that mutations within the sigma-B activator RsbU abrogate PNAG production, suggest that sigma-B plays an important role in the transcriptional activity of the ica locus. A consensus binding site for sigma-B is not present within the ica promoter, so its role may be an indirect one.
Different studies with S. epidermidis show that activation of ica transcription by ethanol is icaR dependent, whereas the activation by ClNa-glucose is rsbU/sigmaB dependent.
The sigB gene is required for salt-induced biofilm production.
It seems that IcaR does not regulate its own expression.
ica expression can be turned on and off by insertion sequence (IS) elements.
>6026|26991683|transcriptional regulator, TetR family|Pseudomonas putida KT2440|TetR
Until now not much is known about specific regulatory proteins involved in pha genes expression.
The ntrB and ntrC genes involved in nitrogen regulation in various bacteria are also involved in the regulation of poly-3-hydroxibutyrate synthesis by ammonia in Azospirillum brasilense SP7.
PhabRPs is a transcriptional activator belonging to AraC-XylS family involved in the expression of the genes required for synthesis of the poly-3-hydroxybutyrate homopolymer.
PhaS from Pseudomonas putida KT2440 is a putative regulatory protein tha shows similarity to the sensor component of the two component regulatory systems, containing a histidine protein kinase and response regulator domain.
GacS is a transmembrane sensor kinase homolog that regulates the alginate and poly-3-hydroxibutyrate polymer production in Actobacter vinelandii.
PHA acumulation from gluconate in Pseudomonas aeruginosa PAO1 requires a functional RpoN sigma factor.
PhaF of Pseudomonas oleovorans is involved in transcriptional regulation of pha genes expression besides to have a structural function binding to PHA granules.
Another member of TetR family that controls the synthesis of PHA (specifically poly-3-hydroxibutyrate) is LuxR from Vibrio harveyi (besides to control bioluminascence).
>6853|19552090|transcriptional regulator|Corynebacterium glutamicum ATCC 13032|TetR
No transcriptional regulation was found for the amtR gene and its expression seems to be constitutive.
When cells grow under nitrogen excess AmtR is bound to its binding sites, upstream the amt gene and the amtB-glnK-glnD operon, repressing expression of the four genes. During nitrogen starvation, AmtR releases from its binding sites allowing the expression of the ammonium uptake systems and of two key proteins involved in the regulation of nitrogen assimilation, GlnK and GlnD. GlnD transfers UMP to GlnK. The complex GlnK-UMP indirectly activates expression of the Glutamine Synthetase I (GSI), the central enzyme for the  assimilation of ammonium under nitrogen limiting conditions.
>6871|19554126|transcriptional regulator|Corynebacterium glutamicum ATCC 13032|TetR
McbR, in the absence of L-methionine, represses the expression of six key enzymes for the biosynthesis of the sulfur containing amino acids L-cysteine and L-methionine including sulfonate utilization and sulfite reduction.
>7937|28872258|transcriptional regulator PhaD|Pseudomonas syringae pv. tomato str. DC3000|TetR
Until now not much was known about specific regulatory proteins involved in pha genes expression.
The ntrB and ntrC genes involved in nitrogen regulation in various bacteria are also involved in the regulation of poly-3-hydroxybutyrate synthesis by ammonia in Azospirillum brasilense SP7.
PhabRPs is a transcriptional activator belonging to the AraC-XylS family involved in the expression of the genes required for the synthesis of the poly-3-hydroxibutyrate homopolymer.
PhaS from Pseudomonas putida KT2440 is a putative regulatory protein that shows similarity to the sensor component of the two-component regulatory systems and  contains a histidine protein kinase and response regulator domain.
GacS is a transmembrane sensor kinase homolog that regulates the alginate and poly-3-hydroxibutyrate polymer production in Actobacter vinelandii.
PHA accumulation from gluconate in Pseudomonas aeruginosa PAO1 requires a functional RpoN sigma factor.
PhaF of Pseudomonas oleovorans is involved in the transcriptional regulation of pha genes expression and has a structural function binding to PHA granules.
Another member of the TetR family that controls the synthesis of PHA (specifically poly-3-hydroxibutyrate) is LuxR from Vibrio harveyi (besides to control bioluminascence).
>9416|O24741|FarA|Streptomyces sp. FRI-5|TetR
FARE covers the farA transcription start site and overlaps the probable -10 region of farA, suggesting that FarA acts as transcriptional repressor of its own synthesis.
FarA is a dimeric DNA binding protein that, in absence of IM-2, recognizes and binds to specific DNA sequences situated in the promoter region of the target gene, repressing its expression. IM-2 binding to FarA causes FarA to dissociate from DNA, which in turn allows the transcription of the target gene to occur.
>9417|P13225|Virulence regulon transcriptional activator virF|Yersinia enterocolitica|AraC
Yop expression requires other factors in addition to VirF.
Y. enterocolitica virulence plasmid, pYV, undergoes a conformational transition between 30 and 37 degrees, a conformational change due to the melting of DNA bends followed by compensatory adjustments in superhelical density. These changes in DNA topology may be the temperature-sensing mechanism for virulence gene expression.
A chromosome-encoded histone-like protein, called YmoA, is involved in the thermoregulation of the yop regulon.