RegulonDB RegulonDB 10.9: Operon Form
   

pyrLBI operon and associated TUs in Escherichia coli K-12 genome




Operon      
Name: pyrLBI
This page displays every known transcription unit of this operon and their known regulation.


Transcription unit       
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 2656651.
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 3044790. 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 3928602. 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 2656651.
Evidence: [ITCR] Inferred through co-regulation
Reference(s): [1] Donahue JP., et al., 1994
[2] Roof WD., et al., 1982
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: [HIPP]
[TIM]
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
Allosteric regulation of RNA-polymerase
  Regulator Function Promoter target of RNApol Growth Conditions Note Evidence Reference
  ppGpp inhibition pyrLp2 nd pyrLp2 (pyrBp2) contains a G+C-rich sequence immediately dowstream of the _10 region that is similar to the discriminator sequence found in stringently controlled promoters Donahue JP,1990 [GEA]
[IMP]
[3]
Evidence: [GEA] Gene expression analysis
[IMP] Inferred from mutant phenotype
Reference(s): [3] Donahue JP., et al., 1990


Transcription unit       
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 2656651.
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 3044790.
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 3928602. 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 2656651.
Based on DNA microarray analysis, the mechanism of bacterial inactivation by carvacrol and citral was studied 28644990. Treatment by both compounds caused membrane damage and activated metabolism through the production of nucleotides required for DNA and RNA synthesis and metabolic processes 28644990. 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 28644990.
Evidence: [ITCR] Inferred through co-regulation
Reference(s): [1] Donahue JP., et al., 1994
[2] Roof WD., et al., 1982
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 31965171 In addition, a series of X-ray crystal structures of the RNAP and pyrL promoter complex were determined 31965171
Evidence: [HIPP]
[IMP]
[TIM]
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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