Disease relevance of uvrB

• The T. thermophilus uvrB gene product was overproduced in Escherichia coli and purified to apparent homogeneity [1].
• The uvrB gene, which plays an essential role in the prokaryotic excision repair, was cloned from an extremely thermophilic bacterium, Thermus thermophilus HB8 [1].
• A promoter associated with the neisserial repeat can be used to transcribe the uvrB gene from Neisseria gonorrhoeae [2].
• The location of the E. coli uvrB gene on the DNA of this transducing phage was established by heteroduplex and restriction-enzyme analyses [3].
• Nitrofurazone, dimethylnitrosamine, cyclophosphamide and 2-acetylaminofluorene were activated to mutagens upon incubation with Drosophila microsomes or 20000 x g supernatant: mutagenicity was observed in Chinese hamster ovary cells, Escherichia coli strains 343/113/R-9 and 343/113/uvrB, and Salmonella typhimurium TA1538 [4].

High impact information on uvrB

• A third promoter, P3, was also detected at -341; transcription from P3 is toward uvrB but terminates in vitro in the region of the LEXA binding site [5].
• Evidence for the inducibility of the uvrB operon [6].
• In contrast to the related uvrA and uvrB genes, uvrC gene expression is characterized by a delayed onset of induction after DNA damaging treatment [7].
• Examination of the nature of the mutations induced by cis-Pt(NH3)2Cl2, by using the LacI system, revealed that base-pair substitutions leading to nonsense mutants are only induced in wild-type cells, suggesting that the intact products of both the uvrB and the recA gene are necessary for the repair responsible for this type of mutagenesis [8].
• An increased frequency (3-fold) of highly focused base substitutions was also observed at 2 sites in the lac operator region (at lacO +6, which is a transition "hotspot" in the spontaneous spectra of both wild type and uvrB- organisms and at the adjacent +5 site) [9].

Chemical compound and disease context of uvrB

• Two uvrB mutant strains of E. coli K-12 (AB1885 and N3-1) were much more sensitive than the isogenic uvrA and uvrC strains to treatment with toluidine blue plus light, suggesting that the uvrB+ gene product was involved in repair of DNA damage induced by the treatment [10].
• As genetic endpoint, black mutation from arg-56 to arg+ was assayed in strain Escherichia coli K-12/343/113/uvrB; this system, in preliminary experiments, was rather sensitive to 8-MOP-induced photodynamic effects [11].
• As opposed to the considerable activity in the Uvr+ strain, formaldehyde was found not to be mutagenically active in an E. coli strain carrying a deletion of the uvrB gene [12].
• The influence of uvrB and umuC genes on the induction of lacI- mutants and nonsense mutants by ethylene oxide (EtO) in the lacI gene of E. coli was studied [13].
• Indicator of genotoxic activity was a pair of streptomycin dependent Escherichia coli strains differing vastly in DNA repair capacity; uvrB/recA vs. uvr+/rec+ [14].

Biological context of uvrB

• An ultraviolet damage repair-deficient mutant (uvrB) contained highly methylated chromosomal and plasmid DNA [15].
• The DNA sequence of the region, which governs the expression of the uvrB gene, has been determined [16].
• A mutant defective in the synthesis of adaptive DNA alkyltransferases and induction of the adaptive response (ada) also showed high methylation and properties similar to that of the dam gene expressing uvrB strain [15].
• Potential sites of interaction within the uvrB regulatory region with regulatory proteins, such as the LexA protein (2) and the UvrC protein (3) are discussed [16].
• The uvrB mutant also was significantly more sensitive than the wild-type strain to killing by low pH, suggesting that the H. pylori nucleotide excision repair (NER) pathway is involved in the repair of acid-induced DNA damage [17].

Associations of uvrB with chemical compounds

• Mutation induction by cis-Pt(NH3)2Cl2 (cisplatin) has been shown to be absent in E.coli strains carrying a deletion of the uvrB gene (1) [18].
• We propose that N6-methyladenine residues are excised by proteins involved in both excision (uvrB) and the adaptive response (ada) DNA repair pathways in B. subtilis [15].
• The two uvrB strains were more sensitive to sodium dodecyl sulfate than the other strains, suggesting that these strains had a defect in the cell surface [10].
• We constructed an isogenic H. pylori uvrB mutant by inserting a kanamycin-resistance cassette into uvrB and verified its proper placement by Southern hybridization [17].
• As with uvrB mutants of other bacteria, the H. pylori uvrB mutant showed a greatly increased sensitivity to the DNA-damaging agents methylmethane sulfonate and ultraviolet radiation [17].

Analytical, diagnostic and therapeutic context of uvrB

• Heteroduplex analysis of the reconstructed F-prime factors confirmed the derivation of the F-prime factors F100 and F152, from the same Hfr, and finally determined the normal E. coli chromosomal sequence in the region between fep and uvrB, containing about 5 min in genetic units and about 246.5 in kilobase units (kb) [19].
• Degenerate oligonucleotide primers based on conserved amino acid residues of bacterial UvrB proteins were used in PCR with genomic DNA from H. pylori strain 84-183, and the 1.3-kb PCR product from this reaction was used as a probe to clone uvrB from an H. pylori genomic library [17].
• Northern blotting and transcriptional fusion assay with lacZ indicated that X. campestris pv. campestris uvrB is expressed constitutively at high levels and cannot be further induced by UV irradiation [20].

References