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| Operon |  |
|---|---|
| Name: | pyrLBI |
| This page displays every known transcription unit of this operon and their known regulation. | |
| Name: | pyrLBI | ||||||||||||||
| Gene(s): | pyrI, pyrB, pyrL Genome Browser M3D Gene expression COLOMBOS | ||||||||||||||
| Note(s): | The pyrLBI operon is regulated primarily by attenuation in response to pyrimidine availability. The pyrLBI operon is controlled by an attenuator that responds to the abundance of UTP by a polymerase-pausing mechanism. pyrL, the gene coding for the PyrL leader peptide, contains a transcriptional terminator preceded by a poly(T) sequence. When UTP levels are low, transcriptional pausing occurs at this poly(T) sequence Turnbough CL,1983. More generally, this sequence leads to UTP-responsive transcriptional control, as transcription terminates there when UTP is abundant and proceeds when UTP levels are low, in a manner that depends on the presence of the terminator Levin HL,1985. The poly(T) tract is also absolutely required for transcriptional termination Liu CG, Turnbough CL,1989. The proposed model for the pyrLBI attenuator is that of polymerase pausing, in which the RNA polymerase may pause at the poly(T) sequence when UTP is lacking, giving the following ribosome a chance to catch up. The proximity of the ribosome then prevents formation of the terminator and premature termination of transcription. In contrast, when UTP is abundant the polymerase races ahead of the ribosome, allowing the terminator hairpin to form and terminating transcription. Partial confirmation of this model comes from the fact that in strains with mutated, slow-moving ribosomes, pyrLBI transcription is far more effectively inhibited by UTP Jensen KF,1988. In addition, although pyrimidine levels have little effect on translation of PyrL, translation of the leader peptide is required for proper regulation by attenuation. Mutatations that block translation of PyrL disrupt attenuation at pyrLBI Roland KL, Powell FE, Turnbough CL,1985. Transcriptional pausing within pyrL is enhanced by NusA Donahue JP,1994. In addition to attenuation, there is evidence of another transcription regulation mechanism, but its participating elements have not been identified Liu CG, Turnbough CL,1989. |
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| Evidence: | [EXP-IEP-COREGULATION] Inferred through co-regulation | ||||||||||||||
| Reference(s): |
[1] Donahue JP., et al., 1994 [2] Roof WD., et al., 1982 |
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| Promoter | |||||||||||||||
| Name: | pyrLp2 | ||||||||||||||
| +1: | 4472553 | ||||||||||||||
| Distance from start of the gene: | 20 | ||||||||||||||
| Sequence: |
| Note(s): |
pyrLp2 is the physiologically important promoter of the pyrLBI operon, with 99% of the transcription starting here Liu C,1993. |
Evidence: |
[COMP-HINF-POSITIONAL-IDENTIFICATION] |
[EXP-IDA-TRANSCRIPTION-INIT-MAPPING] Reference(s): |
[3] Donahue JP., et al., 1990 |
[1] Donahue JP., et al., 1994 [4] Liu C., et al., 1993 Terminator(s) |
| Type: |
rho-independent |
Sequence: |
ggcaaaaaaaAGCCCCTCGATTGAGGGGCTgggaatgggt |
Reference(s): |
[5] Turnbough CL., et al., 1983
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| Allosteric regulation of RNA-polymerase |
| Regulator | Function | Promoter target of RNApol | Growth Conditions | Note | Evidence | Reference | |
|---|---|---|---|---|---|---|---|
| ppGpp | inhibition | pyrLp2 | nd |
[EXP-IEP-GENE-EXPRESSION-ANALYSIS] [EXP-IMP] |
[3] |
| Evidence: |
[EXP-IEP-GENE-EXPRESSION-ANALYSIS] Gene expression analysis [EXP-IMP] Inferred from mutant phenotype |
| Reference(s): | [3] Donahue JP., et al., 1990 |
| Name: | pyrLBI | ||||||||||||||
| Gene(s): | pyrI, pyrB, pyrL Genome Browser M3D Gene expression COLOMBOS | ||||||||||||||
| Note(s): | The pyrLBI operon is regulated primarily by attenuation in response to pyrimidine availability. The pyrLBI operon is controlled by an attenuator that responds to the abundance of UTP by a polymerase-pausing mechanism. pyrL, the gene coding for the PyrL leader peptide, contains a transcriptional terminator preceded by a poly(T) sequence. When UTP levels are low, transcriptional pausing occurs at this poly(T) sequence Turnbough CL,1983. More generally, this sequence leads to UTP-responsive transcriptional control, as transcription terminates there when UTP is abundant and proceeds when UTP levels are low, in a manner that depends on the presence of the terminator Levin HL,1985. The poly(T) tract is also absolutely required for transcriptional termination Liu CG, Turnbough CL,1989. The proposed model for the pyrLBI attenuator is that of polymerase pausing, in which the RNA polymerase may pause at the poly(T) sequence when UTP is lacking, giving the following ribosome a chance to catch up. The proximity of the ribosome then prevents formation of the terminator and premature termination of transcription. In contrast, when UTP is abundant the polymerase races ahead of the ribosome, allowing the terminator hairpin to form and terminating transcription. Partial confirmation of this model comes from the fact that in strains with mutated, slow-moving ribosomes, pyrLBI transcription is far more effectively inhibited by UTP Jensen KF,1988. In addition, although pyrimidine levels have little effect on translation of PyrL, translation of the leader peptide is required for proper regulation by attenuation. Mutatations that block translation of PyrL disrupt attenuation at pyrLBI Roland KL, Powell FE, Turnbough CL,1985. Transcriptional pausing within pyrL is enhanced by NusA Donahue JP,1994. In addition to attenuation, there is evidence of another transcription regulation mechanism, but its participating elements have not been identified Liu CG, Turnbough CL,1989. Based on DNA microarray analysis, the mechanism of bacterial inactivation by carvacrol and citral was studied Chueca B, Pérez-Sáez E, Pagán R, García-Gonzalo D,2017. Treatment by both compounds caused membrane damage and activated metabolism through the production of nucleotides required for DNA and RNA synthesis and metabolic processes Chueca B, Pérez-Sáez E, Pagán R, García-Gonzalo D,2017. A total of 76 and 156 genes demonstrated significant transcriptional differences by carvacrol and citral, respectively. Genes upregulated by carvacrol treatment included the multidrug efflux pump genes acrA and mdtM, genes related to the phage shock response, pspA, pspB, pspC, pspD, pspF, and pspG, and genes whose products are important for biosynthesis of arginine (argC, argG, artJ) and purine nucleotides (purC, purM). Genes upregulated by citral treatment included purH, pyrB, and pyrI. On the other hand, mutations in several differentially expressed genes confirmed the roles of ygaV, yjbO, pspC, sdhA, yejG, and ygaV in mechanisms of inactivation by carvacrol and citral Chueca B, Pérez-Sáez E, Pagán R, García-Gonzalo D,2017. |
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| Evidence: | [EXP-IEP-COREGULATION] Inferred through co-regulation | ||||||||||||||
| Reference(s): |
[1] Donahue JP., et al., 1994 [2] Roof WD., et al., 1982 |
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| Promoter | |||||||||||||||
| Name: | pyrLp1 | ||||||||||||||
| +1: | 4472745 | ||||||||||||||
| Distance from start of the gene: | 212 | ||||||||||||||
| Sequence: |
| Note(s): |
pyrLp1 is the less important promoter of the pyrLBI operon (99% of the transcription beginnings occur at pyrBp2). But if pyrLp1 is removed, a decrement of 15% of transcription initiation is detected Liu C,1993. |
Based on structural and biochemical approaches, the mechanism of reiterative transcription from the pyrL promoter (pyrLBI operon) has been studied Shin Y, Hedglin M, Murakami KS,2020 In addition, a series of X-ray crystal structures of the RNAP and pyrL promoter complex were determined Shin Y, Hedglin M, Murakami KS,2020 Evidence: |
[COMP-HINF-POSITIONAL-IDENTIFICATION] |
[EXP-IDA-TRANSCRIPTION-INIT-MAPPING] [EXP-IMP] Reference(s): |
[3] Donahue JP., et al., 1990 |
[4] Liu C., et al., 1993 [2] Roof WD., et al., 1982 Terminator(s) |
| Type: |
rho-independent |
Sequence: |
ggcaaaaaaaAGCCCCTCGATTGAGGGGCTgggaatgggt |
Reference(s): |
[5] Turnbough CL., et al., 1983
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| Reference(s) |
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|---|---|
[COMP-HINF-POSITIONAL-IDENTIFICATION] Human inference of promoter position