Disease relevance of uvrC

• Regulation of the uvrC gene of Escherichia coli K12: localization and characterization of a damage-inducible promoter [1].
• The Escherichia coli uvrC gene has been cloned into multicopy plasmids from the transducing phage lambda uvrC+ and the structural gene assigned to a 1.9-kb BglII fragment [2].
• Moreover, N-2-aminofluorene-mediated toxicity in the uvrC background was reversed when an additional uvrA mutation was introduced into the strain [3].
• Structure of the Haemophilus influenzae uvr-1+ gene: homology with other uvrC-like genes and characterization of the Haemophilus influenzae uvr-1 and uvr-2 mutations [4].
• Chromosomal location of the Bacillus subtilis aspartokinase II gene and nucleotide sequence of the adjacent genes homologous to uvrC and trx of Escherichia coli [5].

High impact information on uvrC

• This photoreactivation-stimulated in vitro UV mutagenesis was dependent on the excision repair genes uvrA, uvrB, and uvrC and occurred in the absence of DNA replication [6].
• The portion of the uvrC gene encoding the C-terminal half of the protein was fused to the 3' end of the E. coli malE gene (which encodes maltose binding protein), and the fusion protein MBP-C314C was purified and characterized [7].
• Another mutator, designated mutC, maps very near uvrC, at 42 min, but is distinguishable from uvrC, which has no mutator effects [8].
• Similar results were obtained in uvrA and uvrC backgrounds [9].
• A Rec- strain of E. coli ( FP4102 ) which carries the uvrC to his region (42.1-44.1 min) as an F' episome was used to confirm this location [10].

Chemical compound and disease context of uvrC

• In Escherichia coli, the uvrA, uvrB, and uvrC genes are necessary for excision of cyclobutane dimers [11].
• uvrC gene function in excision repair in toluene-treated Escherichia coli [12].
• The survival of phi X174 was evaluated as an index of drug damage and from this we conclude that SR 4233 induces pH-dependent DNA damage in E coli, which is recognized and repaired primarily by the uvrC gene product and by the exonuclease III and endonuclease III gene products [13].

Biological context of uvrC

• Plasmids carrying this PstI fragment, in either orientation (pGY3233, pGY4211) relative to the cloning vehicle, complement uvrC mutants [14].
• The regulatory region of the Escherichia coli uvrC gene has been analysed by the subcloning of appropriate restriction fragments into the promoter probe vector pPV502 [15].
• Analysis of the regulatory elements of the Escherichia coli uvrC gene by construction of operon fusions [15].
• Using the phi X174 RF DNA-E. coli transfection system, we have found that BPDE-I or BPDE-II modified phi X174 RF DNA has much lower transfectivity in uvrA, uvrB, and uvrC mutant cells compared to wild type cells [16].
• We have sequenced the control region of the uvrC protein including two open reading frames (ORF) encoding polypeptides of 28 kd and 23 kd molecular weight [17].

Associations of uvrC with chemical compounds

• We find that the uvrC gene is preceded by three promoters (P1, P2 and P3), identified by heparin-resistant RNA polymerase-DNA complex formation, P2 and P3 promoters are located proximal to the 5' end of the uvrC gene, while the P1 promoter is separated from the uvrC structural gene by an interposed DNA region of more than 1 kb [18].
• Further experiments indicated that chloroquine-induced reversion frequencies were essentially identical in wild-type, recA, umuC and uvrC derivatives of DG1669, as well as in strains carrying the mutation enhancing plasmid pKM101, over a wide range of doses (0-1200 micrograms/plate) [19].

Physical interactions of uvrC

• The addition of the uvrD protein to the incised DNA-uvrABC complex also results in turnover of only the uvrC protein [20].

Other interactions of uvrC

• The uvrA, uvrB, and uvrC genes encode sequences of 442, 60, and 74 amino acids, respectively [21].
• This recruitment process is dependent on the uvrA, uvrC and recA gene products [22].
• To investigate the influence of nucleotide excision repair (NER) on glyoxal-induced mutations, we treated wild-type and NER-deficient (uvrC) Escherichia coli strains with glyoxal, and analyzed mutations in the chromosomal lacI gene [23].
• The deduced amino acid sequence of the distal reading frame exhibits extensive homology with Escherichia coli thioredoxin and that of the proximal one, which overlaps with the ask promoter, is homologous to the deduced product of the E. coli uvrC gene [5].

References