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BaeR DNA-binding transcriptional activator

Synonyms: BaeR-Phosphorylated
Summary:
BaeR has been shown to regulate directly genes involved in drug resistance [1, 5, 8, 9] and indirectly appears to regulate genes involved in several cellular processes, such as flagellum biosynthesis, chemotaxis, and maltose transport [5]. BaeR belongs to the BaeS/BaeR two-component system [2, 10]. Both genes, baeR, encoding the response regulator, and baeS, encoding the sensor kinase, are located at the end of the operon (mdtABCD-baeSR) regulated by BaeR [1]. It has been suggested that BaeS senses envelope disorder [6, 7]. Indole [3, 7] and zinc [6] have been used as inducers of this disorder.
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Transcription factor      
TF conformation(s):
Name Conformation Type TF-Effector Interaction Type Apo/Holo Conformation Evidence (Confirmed, Strong, Weak) References
BaeR-Phosphorylated Functional Covalent Holo [APPH], [BPP], [GEA], [IPI] [1], [2]
Evolutionary Family: OmpR
Sensing class: External-Two-component systems
Connectivity class: Local Regulator
Gene name: baeR
  Genome position: 2164276-2164998
  Length: 723 bp / 240 aa
Operon name: mdtABCD-baeSR
TU(s) encoding the TF:
Transcription unit        Promoter
baeSR
null
mdtABCD-baeSR
mdtAp


Regulon       
Regulated gene(s) acrD, baeR, baeS, mdtA, mdtB, mdtC, mdtD, spy
Multifun term(s) of regulated gene(s) MultiFun Term (List of genes associated to the multifun term)
membrane (6)
Porters (Uni-, Sym- and Antiporters) (4)
two component regulatory systems (external signal) (2)
drug resistance/sensitivity (1)
Transcription related (1)
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Regulated operon(s) acrD, mdtABCD-baeSR, spy
First gene in the operon(s) acrD, mdtA, spy
Simple and complex regulons BaeR,CpxR
Simple and complex regulatory phrases Regulatory phrase (List of promoters regulated by the phrase)
[BaeR,+](3)


Transcription factor regulation    


Transcription factor binding sites (TFBSs) arrangements
      

  Functional conformation Function Promoter Sigma factor Central Rel-Pos Distance to first Gene Genes Sequence LeftPos RightPos Evidence (Confirmed, Strong, Weak) References
  BaeR-Phosphorylated activator acrDp2 Sigma54 -36.5 -81.5 acrD
acattaactcCTTTTTTTCTCCACGATTGGctcgtacctt
2587504 2587523 [BPP], [GEA], [IC] [3]
  BaeR-Phosphorylated activator mdtAp Sigma38 -27.5 -64.5 mdtA, mdtB, mdtC, mdtD, baeS, baeR
cataattcctCCATTTTTCTCCCTTATTGGctggctacac
2153942 2153961 [AIBSCS], [BPP], [GEA] [1], [3], [4], [5]
  BaeR-Phosphorylated activator spyp Sigma70 -157.5 -220.5 spy
gattttgcagAGATTATGAAGAACTATACCggatgactgg
1825836 1825855 [BPP], [HIBSCS], [IC] [6]
  BaeR-Phosphorylated activator spyp Sigma70 -86.5 -149.5 spy
cacttttgcgCCAATTATGGAGAAAAAAAGaaaatttgat
1825765 1825784 [AIBSCS], [BPP], [GEA], [HIBSCS] [5], [6], [7]



High-throughput Transcription factor binding sites (TFBSs)
      

  Functional conformation Function Object name Object type Distance to first Gene Sequence LeftPos RightPos Evidence (Confirmed, Strong, Weak) References
  BaeR-Phosphorylated activator ycaC nd nd nd nd [AISGDTU] nd


Alignment and PSSM for BaeR TFBSs    

Aligned TFBS of BaeR   
  Sequence
  TTTTTCTCCATAATTGGC
  TAGTTCTTCATAATCTCT
  TTTTTCTCCCTTATTGGC
  TTTTTCTCCACGATTGGC

Position weight matrix (PWM).   
A	0	1	0	0	0	0	0	0	0	3	0	2	4	0	0	0	0	0
C	0	0	0	0	0	4	0	3	4	1	1	0	0	0	1	0	1	3
G	0	0	1	0	0	0	0	0	0	0	0	1	0	0	0	3	3	0
T	4	3	3	4	4	0	4	1	0	0	3	1	0	4	3	1	0	1

PWM logo   


 


Evolutionary conservation of regulatory elements    
     Note: Evolutionary conservation of regulatory interactions and promoters is limited to gammaproteobacteria.
TF-target gene evolutionary conservation
Promoter-target gene evolutionary conservation


Evidence    

 [APPH] Assay of protein purified to homogeneity

 [BPP] Binding of purified proteins

 [GEA] Gene expression analysis

 [IPI] Inferred from physical interaction

 [IC] Inferred by curator

 [AIBSCS] Automated inference based on similarity to consensus sequences

 [HIBSCS] Human inference based on similarity to consensus sequences

 [AISGDTU] Automated inference that a single-gene directon is a transcription unit



Reference(s)    

 [1] Baranova N., Nikaido H., 2002, The baeSR two-component regulatory system activates transcription of the yegMNOB (mdtABCD) transporter gene cluster in Escherichia coli and increases its resistance to novobiocin and deoxycholate., J Bacteriol 184(15):4168-76

 [2] Yamamoto K., Hirao K., Oshima T., Aiba H., Utsumi R., Ishihama A., 2005, Functional characterization in vitro of all two-component signal transduction systems from Escherichia coli., J Biol Chem 280(2):1448-56

 [3] Hirakawa H., Inazumi Y., Masaki T., Hirata T., Yamaguchi A., 2005, Indole induces the expression of multidrug exporter genes in Escherichia coli., Mol Microbiol 55(4):1113-26

 [4] Nagakubo S., Nishino K., Hirata T., Yamaguchi A., 2002, The putative response regulator BaeR stimulates multidrug resistance of Escherichia coli via a novel multidrug exporter system, MdtABC., J Bacteriol 184(15):4161-7

 [5] Nishino K., Honda T., Yamaguchi A., 2005, Genome-wide analyses of Escherichia coli gene expression responsive to the BaeSR two-component regulatory system., J Bacteriol 187(5):1763-72

 [6] Yamamoto K., Ogasawara H., Ishihama A., 2008, Involvement of multiple transcription factors for metal-induced spy gene expression in Escherichia coli., J Biotechnol 133(2):196-200

 [7] Raffa RG., Raivio TL., 2002, A third envelope stress signal transduction pathway in Escherichia coli., Mol Microbiol 45(6):1599-611

 [8] Hirakawa H., Nishino K., Hirata T., Yamaguchi A., 2003, Comprehensive studies of drug resistance mediated by overexpression of response regulators of two-component signal transduction systems in Escherichia coli., J Bacteriol 185(6):1851-6

 [9] Hirakawa H., Nishino K., Yamada J., Hirata T., Yamaguchi A., 2003, Beta-lactam resistance modulated by the overexpression of response regulators of two-component signal transduction systems in Escherichia coli., J Antimicrob Chemother 52(4):576-82

 [10] Nagasawa S., Ishige K., Mizuno T., 1993, Novel members of the two-component signal transduction genes in Escherichia coli., J Biochem (Tokyo) 114(3):350-7



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