Disease relevance of uvrD

• The nucleotide sequence of the control region and the presumptive N-terminal portion of the uvrD gene of Escherichia coli K-12 has been determined [1].
• We have subcloned the Escherichia coli uvrD gene under control of the inducible phage lambda PL promoter and report a procedure for the large-scale purification of helicase II protein [2].
• The Salmonella typhimurium LT2 uvrD gene is regulated by the lexA gene product [3].
• Cloning and characterization of the uvrD gene from an extremely thermophilic bacterium, Thermus thermophilus HB8 [4].
• The Haemophilus influenzae mutB+ gene complements Escherichia coli uvrD mutants [5].

High impact information on uvrD

• The Escherichia coli uvrD gene product, helicase II, is required for both methyl-directed mismatch and uvrABC excision repair and is believed to function by unwinding duplex DNA [6].
• A 2.9-kilobase (kb) Pvu II DNA fragment that contains the uvrD gene of Escherichia coli K-12 has been cloned in both low-copy and multiple-copy plasmid vehicles [7].
• Instead, norfloxacin causes DNA damage, as evidenced by the induction of the SOS pathway for DNA repair; the increase in susceptibility to the drug by mutations in genes for DNA repair pathways including recA, recB, and uvrD; and the efficient detergent-induced linearization of plasmid DNA in drug-treated cells [8].
• These results are relevant to the suspected role of the dda protein in phage T4 DNA replication, as well as to its possible role in phage genetic recombination [9].
• Here, we report the cloning and sequencing of two additional P. aeruginosa mismatch repair genes and the characterization, by complementation of deficient strains, of these two putative P. aeruginosa mismatch repair genes (mutL and uvrD) [10].

Chemical compound and disease context of uvrD

• Escherichia coli uvrD mutants with thermosensitive DNA-dependent adenosine triphosphatase I (helicase II) [11].
• Role of the uvrE gene product and of inducible O6-methylguanine removal in the induction of mutations by N-methyl-N'-nitro-N-nitrosoguanidine in Escherichia coli [12].

Biological context of uvrD

• These results indicate that the uvrD gene is induced during the SOS response, and that the expression of the gene may also be regulated by transcription attenuation [1].
• The 1190 base pairs of DNA examined include the likely coding sequence for the first 258 amino acids of the uvrD protein [1].
• The transcription promoter for the uvrD gene was identified upstream of the protein coding region [1].
• Surprisingly, the uvrD deletion completely suppressed the phenotype of a ruvB mutation in a recBCsbcB(C) background [13].
• In addition, the constitutive expression of uvrD was reduced in strains containing either the recA56 mutation or a multi-copy plasmid carrying lexA+ [14].

Anatomical context of uvrD

• Using this assay, DNA damages generated in calf thymus, phi X174 RF, and f1 single-stranded DNA, X-irradiated in phosphate buffer, were easily detectable at 10 rad (0.1 Gy) [15].

Associations of uvrD with chemical compounds

• The interactions of the inhibitory effects of the uvrD, exaA, and recB mutations and chloramphenicol treatment were determined by examining the survival and repair characteristics of the several multiple mutants [16].
• These results indicate that the uvrD mutation inhibits certain rec+lex+-dependent repair processes, including the growth-medium-dependent (Type III) repair of X-ray-induced DNA single-strand breaks, but does not inhibit other rec+lex+-dependent processes that are sensitive to 2,4-dinitrophenol and chloramphenicol [17].
• Alkaline sucrose gradient sedimentation studies indicated that the uvrD strain is deficient in the growth-medium-dependent (Type III) repair of DNA single-strand breaks [17].
• These data suggest that the ultraviolet sensitivity conferred by the uvrD mutation arises from inefficient removal of pyrimidine dimers or from failure to close incision breaks [18].
• We sequenced >250 mutations leading to Rif(r) in D. radiodurans derived spontaneously in wild-type and uvrD (mismatch-repair-deficient) backgrounds and after treatment with N-methyl-N'-nitro-N-nitrosoguanidine (NTG) and 5-azacytidine (5AZ) [19].

Physical interactions of uvrD

• 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 uvrD

• These include three branches that are blocked by the exrA, recB, or uvrD mutation, a fourth branch that is blocked by any of these mutations and is also sensitive to chloramphenicol treatment, and at least one additional branch that is not sensitive to either of these mutations or to chloramphenicol treatment [16].
• It appears, therefore, that the long patches detected in the uvrD mutant were not identical to the recA-dependent patches seen in wild-type cells [21].
• The xerC gene has been localized to the 85-min region of the E. coli chromosome, between cya and uvrD [22].
• Indirect stimulation of recombination in Escherichia coli K-12: dependence on recJ, uvrA, and uvrD [23].
• lon incompatibility associated with mutations causing SOS induction: null uvrD alleles induce an SOS response in Escherichia coli [24].

Analytical, diagnostic and therapeutic context of uvrD

• A cosmid-based genomic DNA library for Thermus thermophilus (Tt) HB8 was constructed, and this was screened by Southern hybridization using a uvrD fragment amplified by PCR as the probe [4].
• On the basis of this sequence analysis, expression of the uvrD gene would be expected to increase after DNA damage or replication inhibition as part of the SOS response, as is reported in the preceding paper [Arthur and Eastlake, Gene 25 (1983) 309-316] [25].
• Neutropenia was induced by 600 rad whole-body irradiation; an infection was induced by the injection of 5 X 10(6) Escherichia coli into the thigh on Day 5 after irradiation [26].

References