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Name: | nrfABCDEFG |
Synonym(s): | OP00279, nrf |
Gene(s): | nrfA, nrfB, nrfC, nrfD, nrfE, nrfF, nrfG Genome Browser M3D Gene expression COLOMBOS |
Note(s): | nrfA operon regulation is complex and is affected by different protein factors. Under anaerobic conditions, FNR activates binding at the -41.5 site, but its activation is repressed by IHF at the -55 site. When nitrate or nitrite is present, NarL is activated (via NarX or NarQ) and, upon binding to its target site, IHF is displaced and derepresses the FNR site to allow its dependent activation. Fis binding plays a central role in the catabolite repression of the nrf operon. Therefore, activation involving FNR, NarL, and IHF is thwarted by Fis when it binds to its target at position -15 and blocks access to the nrf promoter -10 element Browning DF,2005. IHF can also activate the transcription of the nrf operon in an FNR-dependent way when it is bound to the site located at bp -179 from the promoter, but only when NarL and NarP are absent Browning DF,2006 nrfA expression is downregulated by NsrR, which is independent of IHF-dependent regulation Browning DF,2010. NsrR acts as a fine-tuner because it modulates nrfA activity rather than switching it off completely Browning DF,2010. Based on a DNA sampling method, HU and YfhH were determined to be regulating the nrfA gene in vivo Browning DF,2010. HU activates nrfABCDEFG operon expression during exponential growth 19194530. nrfABCDEFG was significantly upregulated in response to quinonas anthraquinone-2-sulfonate (AQSim) reduction and azo dye acid red 18 (AR 18) decolorization under anaerobic conditions 23820558. |
Reference(s): | [1] Hussain H., et al., 1994 |
Promoter | |
Name: | nrfAp |
+1: | 4287671 |
Sigma Factor: | Sigma70 Sigmulon |
Distance from start of the gene: | 93 |
Sequence: |
atgcacttacaattgattaaagacaacattcacagtgtggttatttgttacacataggggCgagcaatgtcatgacagtgt -35 -10 +1 |
Note(s): | Nitrate causes repression of the nrfAp promoter in a NarL- or a NarP-protein-dependent way, while repression of the same promoter by nitrite is mainly dependent on the NarP protein Stewart V,2003 |
Evidence: |
[IMP] [TIM] |
Reference(s): |
[2] Darwin A., et al., 1993 [3] Tyson KL., et al., 1994 |
Type | Transcription factor | Function | Promoter | Binding Sites | Growth Conditions | Evidence (Confirmed, Strong, Weak) | Reference(s) | |||
---|---|---|---|---|---|---|---|---|---|---|
LeftPos | RightPos | Central Rel-Pos | Sequence | |||||||
proximal | FNR1 | activator | nrfAp | 4287623 | 4287636 | -41.5 | gcacttacaaTTGATTAAAGACAAcattcacagt | nd | [BCE], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(GEA/ROMA)], [GEA] | [10], [11] |
Type | Transcription factor | Function | Promoter | Binding Sites | Growth Conditions | Evidence (Confirmed, Strong, Weak) | Reference(s) | |||
---|---|---|---|---|---|---|---|---|---|---|
LeftPos | RightPos | Central Rel-Pos | Sequence | |||||||
remote | IHF1 | activator | nrfAp | 4287538 | 4287550 | -127.0 | tgattaattcTTTGAGGAACATGcagttatgca | nd | [AIBSCS], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [4], [5], [6] |
Type | Transcription factor | Function | Promoter | Binding Sites | Growth Conditions | Evidence (Confirmed, Strong, Weak) | Reference(s) | |||
---|---|---|---|---|---|---|---|---|---|---|
LeftPos | RightPos | Central Rel-Pos | Sequence | |||||||
proximal | NarL-Phosphorylated | activator | nrfAp | 4287584 | 4287599 | -79.0 | gaggaagataCTGACTAACTCTAAAGtggtatttta | nd | [AIBSCS], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [3], [9], [10], [11], [12], [13] |
proximal | NarL-Phosphorylated2 | activator | nrfAp | 4287593 | 4287608 | -70.0 | actgactaacTCTAAAGTGGTATTTTacatgcactt | nd | [APIORCISFBSCS], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [3], [9], [10], [11], [12], [13] |
proximal | NarL-Phosphorylated3 | activator | nrfAp | 4287613 | 4287628 | -50.0 | tattttacatGCACTTACAATTGATTaaagacaaca | nd | [APIORCISFBSCS], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [3], [9], [11], [12], [13] |
Type | Transcription factor | Function | Promoter | Binding Sites | Growth Conditions | Evidence (Confirmed, Strong, Weak) | Reference(s) | |||
---|---|---|---|---|---|---|---|---|---|---|
LeftPos | RightPos | Central Rel-Pos | Sequence | |||||||
proximal | NarL-Phosphorylated1 | repressor | nrfAp | 4287613 | 4287628 | -50.0 | tattttacatGCACTTACAATTGATTaaagacaaca | nd | [APIORCISFBSCS], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [3], [9], [11], [12], [13] |
proximal | NarL-Phosphorylated2 | repressor | nrfAp | 4287641 | 4287656 | -22.0 | agacaacattCACAGTGTGGTTATTTgttacacata | nd | [APIORCISFBSCS], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [3], [9], [11], [12], [13] |
Type | Transcription factor | Function | Promoter | Binding Sites | Growth Conditions | Evidence (Confirmed, Strong, Weak) | Reference(s) | |||
---|---|---|---|---|---|---|---|---|---|---|
LeftPos | RightPos | Central Rel-Pos | Sequence | |||||||
proximal | NarP-Phosphorylated | activator | nrfAp | 4287584 | 4287599 | -79.0 | gaggaagataCTGACTAACTCTAAAGtggtatttta | nd | [APIORCISFBSCS], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [3], [9], [10], [11], [12], [13] |
proximal | NarP-Phosphorylated2 | activator | nrfAp | 4287593 | 4287608 | -70.0 | actgactaacTCTAAAGTGGTATTTTacatgcactt | nd | [APIORCISFBSCS], [BPP], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [3], [9], [10], [11], [12], [13] |
Type | Transcription factor | Function | Promoter | Binding Sites | Growth Conditions | Evidence (Confirmed, Strong, Weak) | Reference(s) | |||
---|---|---|---|---|---|---|---|---|---|---|
LeftPos | RightPos | Central Rel-Pos | Sequence | |||||||
remote | NsrR | repressor | nrfAp | 4287545 | 4287556 | -121.0 | ttctttgaggAACATGCAGTTAtgcatgctgt | nd | [APIORCISFBSCS], [CV(GEA/ROMA)], [GEA] | [7], [8] |
proximal | NsrR | repressor | nrfAp | 4287599 | 4287617 | -63.0 | taactctaaaGTGGTATTTTACATGCACTtacaattgat | nd | [APIORCISFBSCS], [BCE], [CV(CHIP-SV/GEA/ROMA)], [CV(CHIP-SV/SM)], [CV(GEA/ROMA)], [CV(GEA/ROMA/SM)], [GEA], [SM] | [8], [14] |
Note(s): |
1nrf regulation is totally dependent on FNR at this site (-41.5) under anaerobic conditions. FNR and NarL/NarP act by promoting the open complex formation by RNA polymerase at the nrf promoter. Although it seems that NarL and FNR can bind to their targets independently, NarL is unable to activate the nrf promoter in the absence of FNR Browning DF,2005. Based on DNase I footprinting Browning DF,2005 suggest that IHF alters the binding of FNR without displacing it from its site. In adittion, NarL binding prevents IHF binding but has little or no effect on FNR or Fis binding.1Fis binding to this site weakly represses the nrfAp promoter and strongly represses acsP1, a promoter that overlaps and is divergent to nrfAp. Either IHF or Fis can repress FNR-dependent open complex formation. NarL binding to its target reverses IHF-dependent repression but does not relieve Fis-dependent repression Browning DF,2005.1The regulatory effect of FlhDC in nrfA operon transcription has been proved only by microarray analysis by Pruss BM,2001.1IHF, located at -127 from the nrfAp promoter, is necessary to activate the FNR-dependent transcription of the nrfABCDEFG operon , but only in the absence of NarL/NarP Browning DF,20061IHF binding to a site located -55 bp from the promoter weakly represses the nrfAp promoter and strongly represses acsP1, a promoter that overlaps and is divergent to nrfAp. NarL and IHF cannot bind together, contrary to other protein regulators that can bind together to form ternary complexes. Fis binds independently to FNR and IHF. Browning DF,2005 supposes that Fis blocks access of RNAP to the nrf promoter. Based on DNase footprinting Browning DF,2005 it is suggested that IHF alters the binding of FNR without displacing it from its site. In addition, NarL binding prevents IHF binding but has little or no effect on FNR or Fis binding. Either Fis or IHF at -55 can repress FNR-dependent open complex formation. NarL binding to its target reverses IHF-dependent repression but does not relieve Fis-dependent repression Browning DF,2005 2The maximum nrfA expression is achieved at low nitrate concentrations through NarP and mainly through NarL. Wang and Gunsalus Wang H,2000 reported that the nitrite is a less effective inductor of nrfA expression, although in a earlier report Page et al. 2173895 reported that this molecule was the primary signal. The sites at -70 and -79 are recognized by NarL and NarP, but NarL has the highest affinity for them. nrf expression is increased in response to nitrite or nitrate ions by NarL or NarP. FNR and NarL/NarP act by promoting open complex formation by RNAP at the nrf promoter. Although it seems that NarL and FNR can bind to their targets independently, NarL is unable to activate the nrf promoter in the absence of FNR Browning DF,2005. NarL and IHF cannot bind together; the other protein regulators can bind together to form ternary complexes. Fis binds independently of FNR and IHF. Browning DF,2005 supposed that Fis blocks access of RNAP to the nrf promoter. 3At low levels of nitrate, NarL activates nrfA expression and at high levels of nitrate NarL represses it.1At low levels of nitrate, NarL activates nrfA expression and at high levels of nitrate NarL represses it. 2The -22 and -50 NarL sites are needed for optimal repression of nrfA expression. At high nitrate concentrations NarL can repress nrfA expression, but NarP cannot Wang H,20002NarP appears to weakly antagonize the activation of nrfA by NarL at low nitrate concentrations Wang H,2000 nrf expression is increased in response to nitrite or nitrate ions by NarL or NarP. FNR and NarL/NarP act by promoting open complex formation by RNAP at the nrf promoter. Although it seems that NarL and FNR can bind to their targets independently, NarL is unable to activate the nrf promoter in the absence of FNR Browning DF,2005. NarL and IHF cannot bind together, and the other protein regulator can bind together to form ternary complexes. Fis binds independently of FNR and IHF. Browning DF,2005 supposed that Fis block access of RNAP to the nrf promoter. 1IHF, located at -127 from the nrfAp promoter, is necessary to activate the FNR-dependent transcription of the nrfABCDEFG operon , but only in the absence of NarL/NarP Browning DF,2006 5NarP appears to weakly antagonize the activation of nrfA by NarL at low nitrate concentrations Wang H,2000 nrf expression is increased in response to nitrite or nitrate ions by NarL or NarP. FNR and NarL/NarP act by promoting open complex formation by RNAP at the nrf promoter. Although it seems that NarL and FNR can bind to their targets independently, NarL is unable to activate the nrf promoter in the absence of FNR Browning DF,2005. NarL and IHF cannot bind together, and the other protein regulator can bind together to form ternary complexes. Fis binds independently of FNR and IHF. Browning DF,2005 supposed that Fis block access of RNAP to the nrf promoter. 6The maximum nrfA expression is achieved at low nitrate concentrations through NarP and mainly through NarL. Wang and Gunsalus Wang H,2000 reported that the nitrite is a less effective inductor of nrfA expression, although in a earlier report Page et al. 2173895 reported that this molecule was the primary signal. The sites at -70 and -79 are recognized by NarL and NarP, but NarL has the highest affinity for them. nrf expression is increased in response to nitrite or nitrate ions by NarL or NarP. FNR and NarL/NarP act by promoting open complex formation by RNAP at the nrf promoter. Although it seems that NarL and FNR can bind to their targets independently, NarL is unable to activate the nrf promoter in the absence of FNR Browning DF,2005. NarL and IHF cannot bind together; the other protein regulators can bind together to form ternary complexes. Fis binds independently of FNR and IHF. Browning DF,2005 supposed that Fis blocks access of RNAP to the nrf promoter. 8IHF binding to a site located -55 bp from the promoter weakly represses the nrfAp promoter and strongly represses acsP1, a promoter that overlaps and is divergent to nrfAp. NarL and IHF cannot bind together, contrary to other protein regulators that can bind together to form ternary complexes. Fis binds independently to FNR and IHF. Browning DF,2005 supposes that Fis blocks access of RNAP to the nrf promoter. Based on DNase footprinting Browning DF,2005 it is suggested that IHF alters the binding of FNR without displacing it from its site. In addition, NarL binding prevents IHF binding but has little or no effect on FNR or Fis binding. Either Fis or IHF at -55 can repress FNR-dependent open complex formation. NarL binding to its target reverses IHF-dependent repression but does not relieve Fis-dependent repression Browning DF,2005 9At low levels of nitrate, NarL activates nrfA expression and at high levels of nitrate NarL represses it. 10At low levels of nitrate, NarL activates nrfA expression and at high levels of nitrate NarL represses it. 11nrf regulation is totally dependent on FNR at this site (-41.5) under anaerobic conditions. FNR and NarL/NarP act by promoting the open complex formation by RNA polymerase at the nrf promoter. Although it seems that NarL and FNR can bind to their targets independently, NarL is unable to activate the nrf promoter in the absence of FNR Browning DF,2005. Based on DNase I footprinting Browning DF,2005 suggest that IHF alters the binding of FNR without displacing it from its site. In adittion, NarL binding prevents IHF binding but has little or no effect on FNR or Fis binding. 12The -22 and -50 NarL sites are needed for optimal repression of nrfA expression. At high nitrate concentrations NarL can repress nrfA expression, but NarP cannot Wang H,2000 13Fis binding to this site weakly represses the nrfAp promoter and strongly represses acsP1, a promoter that overlaps and is divergent to nrfAp. Either IHF or Fis can repress FNR-dependent open complex formation. NarL binding to its target reverses IHF-dependent repression but does not relieve Fis-dependent repression Browning DF,2005. 14The regulatory effect of FlhDC in nrfA operon transcription has been proved only by microarray analysis by Pruss BM,2001. |
RNA cis-regulatory element | ![]() |
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Regulation, transcriptional elongation | |
Attenuator type: | Translational |
Strand: | forward |
Structure type | Energy | LeftPos | RightPos | Sequence (RNA-strand) | |
---|---|---|---|---|---|
terminator | -9.6 | 4287726 | 4287744 | aataaaaaccGCCATTGCAACAATGGCGcaattcggat |
Notes: "The provided "Sequence" is that of the RNA strand, i.e. U's are shown instead of T's and regulators on the reverse strand will appear as the reverse complement of the sequence delimited by LeftPos-RigtPos" |
Reference(s) |
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