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| Operon |  |
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| Name: | purHD |
| This page displays every known transcription unit of this operon and their known regulation. | |
| Name: | purHD | |||||||||
| Synonym(s): | OP00078, purH | |||||||||
| Gene(s): | purD, purH Genome Browser M3D Gene expression COLOMBOS | |||||||||
| Note(s): | The site for the RbsR transcriptional regulator in the purHD operon was identified based on genomic Selex analysis Shimada T,2013 The deletion of the Fis DNA binding sites located upstream of the purHp promoter enhances the inhibition of purHp via transcription-coupled DNA supercoiling (TCDS) in the early log phase. Fis appears to block supercoiling diffusion close to purHp Dages S, Zhi X, Leng F,2020. 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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| Reference(s): | [1] Aiba A., et al., 1989 | |||||||||
| Promoter | ||||||||||
| Name: | purHp | |||||||||
| +1: | 4207627 | |||||||||
| Sigma Factor: | Sigma70 Sigmulon | |||||||||
| Distance from start of the gene: | 95 | |||||||||
| Sequence: |
tcaccattgaaagagaaaaattcgcgagcgttgcgcaaacgttttcgttacaatgcgggcGaaaaataaggatgccccgtt -35 -10 +1 |
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| Evidence: |
[ICWHO] [TIM] |
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| Reference(s): |
[1] Aiba A., et al., 1989 [2] He B., et al., 1990 [3] Huerta AM., et al., 2003 |
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| Type | Transcription factor | Function | Promoter | Binding Sites | Growth Conditions | Evidence (Confirmed, Strong, Weak) | Reference(s) | |||
|---|---|---|---|---|---|---|---|---|---|---|
| LeftPos | RightPos | Central Rel-Pos | Sequence | |||||||
| remote | PhoP-phosphorylated | activator | purHp | 4208098 | 4208114 | -479.0 | taaacttcgtAATGAATTACGTGTTCActcttgagac | nd | [GEA], [AIBSCS] | [4] |
| Type | Transcription factor | Function | Promoter | Binding Sites | Growth Conditions | Evidence (Confirmed, Strong, Weak) | Reference(s) | |||
|---|---|---|---|---|---|---|---|---|---|---|
| LeftPos | RightPos | Central Rel-Pos | Sequence | |||||||
| proximal | PurR-hypoxanthine | repressor | purHp | 4207640 | 4207655 | -20.5 | cgcgagcgttGCGCAAACGTTTTCGTtacaatgcgg | nd | [GEA], [AIBSCS], [APIORCISFBSCS], [BPP] | [2], [5] |
| RNA cis-regulatory element | |
|---|
| Regulation, transcriptional elongation | |
| Attenuator type: | Transcriptional |
| Strand: | reverse |
| Structure type | Energy | LeftPos | RightPos | Sequence (RNA-strand) | |
|---|---|---|---|---|---|
| terminator | -14.9 | 4207585 | 4207630 | ttacaatgcgGGCGAAAAATAAGGATGCCCCGTTAGGGGCGTTAGCTGAGTTTTTcgcgaaaaat | |
| anti-terminator | -7.3 | 4207607 | 4207636 | ttttcgttacAATGCGGGCGAAAAATAAGGATGCCCCGTtaggggcgtt | |
| anti-anti-terminator | -15.2 | 4207625 | 4207667 | aagagaaaaaTTCGCGAGCGTTGCGCAAACGTTTTCGTTACAATGCGGGCGAaaaataagga |
| 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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|---|---|
[ICWHO] Inferred computationally without human oversight