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Artykuły w czasopismach na temat „UvrC”

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Data publikacji: 6 września 2023

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1

Moolenaar, Geri F., Celine Moorman i Nora Goosen. "Role of the Escherichia coli Nucleotide Excision Repair Proteins in DNA Replication". Journal of Bacteriology 182, nr 20 (15.10.2000): 5706–14. http://dx.doi.org/10.1128/jb.182.20.5706-5714.2000.

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ABSTRACT DNA polymerase I (PolI) functions both in nucleotide excision repair (NER) and in the processing of Okazaki fragments that are generated on the lagging strand during DNA replication.Escherichia coli cells completely lacking the PolI enzyme are viable as long as they are grown on minimal medium. Here we show that viability is fully dependent on the presence of functional UvrA, UvrB, and UvrD (helicase II) proteins but does not require UvrC. In contrast, ΔpolA cells grow even better when theuvrC gene has been deleted. Apparently UvrA, UvrB, and UvrD are needed in a replication backup system that replaces the PolI function, and UvrC interferes with this alternative replication pathway. With specific mutants of UvrC we could show that the inhibitory effect of this protein is related to its catalytic activity that on damaged DNA is responsible for the 3′ incision reaction. Specific mutants of UvrA and UvrB were also studied for their capacity to support the PolI-independent replication. Deletion of the UvrC-binding domain of UvrB resulted in a phenotype similar to that caused by deletion of the uvrC gene, showing that the inhibitory incision activity of UvrC is mediated via binding to UvrB. A mutation in the N-terminal zinc finger domain of UvrA does not affect NER in vivo or in vitro. The same mutation, however, does give inviability in combination with the ΔpolA mutation. Apparently the N-terminal zinc-binding domain of UvrA has specifically evolved for a function outside DNA repair. A model for the function of the UvrA, UvrB, and UvrD proteins in the alternative replication pathway is discussed.

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2

LeCuyer, Brian E., Alison K. Criss i H. Steven Seifert. "Genetic Characterization of the Nucleotide Excision Repair System of Neisseria gonorrhoeae". Journal of Bacteriology 192, nr 3 (20.11.2009): 665–73. http://dx.doi.org/10.1128/jb.01018-09.

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ABSTRACT Nucleotide excision repair (NER) is universally used to recognize and remove many types of DNA damage. In eubacteria, the NER system typically consists of UvrA, UvrB, UvrC, the UvrD helicase, DNA polymerase I, and ligase. In addition, when DNA damage blocks transcription, transcription-repair coupling factor (TRCF), the product of the mfd gene, recruits the Uvr complex to repair the damage. Previous work using selected mutants and assays have indicated that pathogenic Neisseria spp. carry a functional NER system. In order to comprehensively examine the role of NER in Neisseria gonorrhoeae DNA recombination and repair processes, the predicted NER genes (uvrA, uvrB, uvrC, uvrD, and mfd) were each disrupted by a transposon insertion, and the uvrB and uvrD mutants were complemented with a copy of each gene in an ectopic locus. Each uvr mutant strain was highly sensitive to UV irradiation and also showed sensitivity to hydrogen peroxide killing, confirming that all of the NER genes in N. gonorrhoeae are functional. The effect of RecA expression on UV survival was minor in uvr mutants but much larger in the mfd mutant. All of the NER mutants demonstrated wild-type levels of pilin antigenic variation and DNA transformation. However, the uvrD mutant exhibited higher frequencies of PilC-mediated pilus phase variation and spontaneous mutation, a finding consistent with a role for UvrD in mismatch repair. We conclude that NER functions are conserved in N. gonorrhoeae and are important for the DNA repair capabilities of this strict human pathogen.

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3

Humann, Jodi L., Hope T. Ziemkiewicz, Svetlana N. Yurgel i Michael L. Kahn. "Regulatory and DNA Repair Genes Contribute to the Desiccation Resistance of Sinorhizobium meliloti Rm1021". Applied and Environmental Microbiology 75, nr 2 (21.11.2008): 446–53. http://dx.doi.org/10.1128/aem.02207-08.

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ABSTRACT Sinorhizobium meliloti can form a nitrogen-fixing symbiotic relationship with alfalfa after bacteria in the soil infect emerging root hairs of the growing plant. To be successful at this, the bacteria must be able to survive in the soil between periods of active plant growth, including when conditions are dry. The ability of S. meliloti to withstand desiccation has been known for years, but genes that contribute to this phenotype have not been identified. Transposon mutagenesis was used in combination with novel screening techniques to identify four desiccation-sensitive mutants of S. meliloti Rm1021. DNA sequencing of the transposon insertion sites identified three genes with regulatory functions (relA, rpoE2, and hpr) and a DNA repair gene (uvrC). Various phenotypes of the mutants were determined, including their behavior on several indicator media and in symbiosis. All of the mutants formed an effective symbiosis with alfalfa. To test the hypothesis that UvrC-related excision repair was important in desiccation resistance, uvrA, uvrB, and uvrC deletion mutants were also constructed. These strains were sensitive to DNA damage induced by UV light and 4-NQO and were also desiccation sensitive. These data indicate that uvr gene-mediated DNA repair and the regulation of stress-induced pathways are important for desiccation resistance.

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4

Hall, Barry G. "Genetics of selection-induced mutations: I. uvrA, uvrB, uvrC, and uvrD are selection-induced specific mutator loci". Journal of Molecular Evolution 40, nr 1 (styczeń 1995): 86–93. http://dx.doi.org/10.1007/bf00166599.

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5

Thomas, D. C., M. Levy i A. Sancar. "Amplification and purification of UvrA, UvrB, and UvrC proteins of Escherichia coli." Journal of Biological Chemistry 260, nr 17 (sierpień 1985): 9875–83. http://dx.doi.org/10.1016/s0021-9258(17)39318-3.

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6

Selby, Christopher P., Laura A. Lindsey-Boltz, Yanyan Yang i Aziz Sancar. "Mycobacteria excise DNA damage in 12- or 13-nucleotide-long oligomers by prokaryotic-type dual incisions and performs transcription-coupled repair". Journal of Biological Chemistry 295, nr 50 (21.10.2020): 17374–80. http://dx.doi.org/10.1074/jbc.ac120.016325.

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In nucleotide excision repair, bulky DNA lesions such as UV-induced cyclobutane pyrimidine dimers are removed from the genome by concerted dual incisions bracketing the lesion, followed by gap filling and ligation. So far, two dual-incision patterns have been discovered: the prokaryotic type, which removes the damage in 11–13-nucleotide-long oligomers, and the eukaryotic type, which removes the damage in 24–32-nucleotide-long oligomers. However, a recent study reported that the UvrC protein of Mycobacterium tuberculosis removes damage in a manner analogous to yeast and humans in a 25-mer oligonucleotide arising from incisions at 15 nt from the 3´ end and 9 nt from the 5´ end flanking the damage. To test this model, we used the in vivo excision assay and the excision repair sequencing genome-wide repair mapping method developed in our laboratory to determine the repair pattern and genome-wide repair map of Mycobacterium smegmatis. We find that M. smegmatis, which possesses homologs of the Escherichia coli uvrA, uvrB, and uvrC genes, removes cyclobutane pyrimidine dimers from the genome in a manner identical to the prokaryotic pattern by incising 7 nt 5´ and 3 or 4 nt 3´ to the photoproduct, and performs transcription-coupled repair in a manner similar to E. coli.

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7

McCready, S., i L. Marcello. "Repair of UV damage in Halobacterium salinarum". Biochemical Society Transactions 31, nr 3 (1.06.2003): 694–98. http://dx.doi.org/10.1042/bst0310694.

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Halobacterium is one of the few known Archaea that tolerates high levels of sunlight in its natural environment. Photoreactivation is probably its most important strategy for surviving UV irradiation and we have shown that both of the major UV photoproducts, cyclobutane pyrimidine dimers (CPDs) and (6–4) photoproducts, can be very efficiently repaired by photoreactivation in this organism. There are two putative photolyase gene homologues in the published genome sequence of Halobacterium sp. NRC-1. We have made a mutant deleted in one of these, phr2, and confirmed that this gene codes for a CPD photolyase. (6–4) photoproducts are still photoreactivated in the mutant so we are currently establishing whether the other homologue, phr1, codes for a (6–4) photolyase. We have also demonstrated an excision repair capacity that operates in the absence of visible light but the nature of this pathway is not yet known. There is probably a bacteria-type excision-repair mechanism, since homologues of uvrA, uvrB, uvrC and uvrD have been identified in the Halobacterium genome. However, there are also homologues of eukaryotic nucleotide-excision-repair genes (Saccharomy cescerevisiae RAD3, RAD25 and RAD2) so there may be multiple repair mechanisms for UV damage in Halobacterium.

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8

SaiSree, L., Manjula Reddy i J. Gowrishankar. "lon Incompatibility Associated with Mutations Causing SOS Induction: Null uvrD Alleles Induce an SOS Response in Escherichia coli". Journal of Bacteriology 182, nr 11 (1.06.2000): 3151–57. http://dx.doi.org/10.1128/jb.182.11.3151-3157.2000.

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ABSTRACT The uvrD gene in Escherichia coli encodes a 720-amino-acid 3′-5′ DNA helicase which, although nonessential for viability, is required for methyl-directed mismatch repair and nucleotide excision repair and furthermore is believed to participate in recombination and DNA replication. We have shown in this study that null mutations in uvrD are incompatible withlon, the incompatibility being a consequence of the chronic induction of SOS in uvrD strains and the resultant accumulation of the cell septation inhibitor SulA (which is a normal target for degradation by Lon protease). uvrD-lonincompatibility was suppressed by sulA,lexA3(Ind−), or recA (Def) mutations. Other mutations, such as priA, dam,polA, and dnaQ (mutD) mutations, which lead to persistent SOS induction, were also lonincompatible. SOS induction was not observed in uvrC andmutH (or mutS) mutants defective, respectively, in excision repair and mismatch repair. Nor wasuvrD-mediated SOS induction abolished by mutations in genes that affect mismatch repair (mutH), excision repair (uvrC), or recombination (recB andrecF). These data suggest that SOS induction inuvrD mutants is not a consequence of defects in these three pathways. We propose that the UvrD helicase participates in DNA replication to unwind secondary structures on the lagging strand immediately behind the progressing replication fork, and that it is the absence of this function which contributes to SOS induction inuvrD strains.

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9

Tang, M. S., i L. Ross. "Single-strand breakage of DNA in UV-irradiated uvrA, uvrB, and uvrC mutants of Escherichia coli." Journal of Bacteriology 161, nr 3 (1985): 933–38. http://dx.doi.org/10.1128/jb.161.3.933-938.1985.

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10

Thakur, Manoj, Sugith Badugu i Kalappa Muniyappa. "UvrA and UvrC subunits of the Mycobacterium tuberculosis UvrABC excinuclease interact independently of UvrB and DNA". FEBS Letters 594, nr 5 (24.11.2019): 851–63. http://dx.doi.org/10.1002/1873-3468.13671.

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11

Eriksson, Anders R. B., Robert A. Andersson, Minna Pirhonen i E. Tapio Palva. "Two-Component Regulators Involved in the Global Control of Virulence in Erwinia carotovora subsp. carotovora". Molecular Plant-Microbe Interactions® 11, nr 8 (sierpień 1998): 743–52. http://dx.doi.org/10.1094/mpmi.1998.11.8.743.

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Production of extracellular, plant cell wall degrading enzymes, the main virulence determinants of the plant pathogen Erwinia carotovora subsp. carotovora, is coordinately controlled by a complex regulatory network. Insertion mutants in the exp (extracellular enzyme production) loci exhibit pleiotropic defects in virulence and the growth-phase-dependent transcriptional activation of genes encoding extracellular enzymes. Two new exp mutations, designated expA and expS, were characterized. Introduction of the corresponding wild-type alleles to the mutants complemented both the lack of virulence and the impaired production of plant cell wall degrading enzymes. The expA gene was shown to encode a 24-kDa polypeptide that is structurally and functionally related to the uvrY gene product of Escherichia coli and the GacA response regulator of Pseudomonas fluorescens. Functional similarity of expA and uvrY was demonstrated by genetic complementation. The expA gene is organized in an operon together with a uvrC-like gene, identical to the organization of uvrY and uvrC in E. coli. The unlinked expS gene encodes a putative sensor kinase that shows 92% identity to the recently described rpfA gene product from another E. carotovora subsp. carotovora strain. Our data suggest that ExpS and ExpA are members of two-component sensor kinase and response regulator families, respectively. These two proteins might interact in controlling virulence gene expression in E. carotovora subsp. carotovora.

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12

Szwarocka, Sylwia T., Paweł Stączek i Paweł Parniewski. "Chromosomal model for analysis of a long CTG/CAG tract stability in wild-type Escherichia coli and its nucleotide excision repair mutants". Canadian Journal of Microbiology 53, nr 7 (lipiec 2007): 860–68. http://dx.doi.org/10.1139/w07-047.

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Many human hereditary neurological diseases, including fragile X syndrome, myotonic dystrophy, and Friedreich’s ataxia, are associated with expansions of the triplet repeat sequences (TRS) (CGG/CCG, CTG/CAG, and GAA/TTC) within or near specific genes. Mechanisms that mediate mutations of TRS include DNA replication, repair, and gene conversion and (or) recombination. The involvement of the repair systems in TRS instability was investigated in Escherichia coli on plasmid models, and the results showed that the deficiency of some nucleotide excision repair (NER) functions dramatically affects the stability of long CTG inserts. In such models in which there are tens or hundreds of plasmid molecules in each bacterial cell, repetitive sequences may interact between themselves and according to a recombination hypothesis, which may lead to expansions and deletions within such repeated tracts. Since one cannot control interaction between plasmids, it is also sometimes difficult to give precise interpretation of the results. Therefore, using modified lambda phage (λInCh), we have constructed a chromosomal model to study the instability of trinucleotide repeat sequences in E. coli. We have shown that the stability of (CTG/CAG)68 tracts in the bacterial chromosome is influenced by mutations in NER genes in E. coli. The absence of the uvrC or uvrD gene products greatly enhances the instability of the TRS in the chromosome, whereas the lack of the functional UvrA or UvrB proteins causes substantial stabilization of (CTG/CAG) tracts.

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13

Qiu, Xiaoyun, George W. Sundin, Benli Chai i James M. Tiedje. "Survival of Shewanella oneidensis MR-1 after UV Radiation Exposure". Applied and Environmental Microbiology 70, nr 11 (listopad 2004): 6435–43. http://dx.doi.org/10.1128/aem.70.11.6435-6443.2004.

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ABSTRACT We systematically investigated the physiological response as well as DNA damage repair and damage tolerance in Shewanella oneidensis MR-1 following UVC, UVB, UVA, and solar light exposure. MR-1 showed the highest UVC sensitivity among Shewanella strains examined, with D37 and D10 values of 5.6 and 16.5% of Escherichia coli K-12 values. Stationary cells did not show an increased UVA resistance compared to exponential-phase cells; instead, they were more sensitive at high UVA dose. UVA-irradiated MR-1 survived better on tryptic soy agar than Luria-Bertani plates regardless of the growth stage. A 20% survival rate of MR-1 was observed following doses of 3.3 J of UVC m−2, 568 J of UVB m−2, 25 kJ of UVA m−2, and 558 J of solar UVB m−2, respectively. Photoreactivation conferred an increased survival rate to MR-1 of as much as 177- to 365-fold, 11- to 23-fold, and 3- to 10-fold following UVC, UVB, and solar light irradiation, respectively. A significant UV mutability to rifampin resistance was detected in both UVC- and UVB-treated samples, with the mutation frequency in the range of 10−5 to 10−6. Unlike in E. coli, the expression levels of the nucleotide excision repair (NER) component genes uvrA, uvrB, and uvrD were not damage inducible in MR-1. Complementation of Pseudomonas aeruginosa UA11079 (uvrA deficient) with uvrA of MR-1 increased the UVC survival of this strain by more than 3 orders of magnitude. Loss of damage inducibility of the NER system appears to contribute to the high sensitivity of this bacterium to UVR as well as to other DNA-damaging agents.

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14

Jeruzalmi, David. "Inner Workings of the UvrA·UvrB DNA Damage Sensor during Bacterial Nucleotide Excision Repair". Acta Crystallographica Section A Foundations and Advances 70, a1 (5.08.2014): C453. http://dx.doi.org/10.1107/s2053273314095461.

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Efficient elimination of DNA lesions by the nucleotide excision repair (NER) pathway is critical for all organisms. In bacteria, the NER pathway is implemented by the successive action of three proteins, UvrA, UvrB and UvrC via a series of large and dynamic multi-protein complexes. A large number of studies have defined three major stages associated with the early steps of the NER pathway. In stage 1, a large (300-400 kDa) complex of the UvrA and UvrB proteins (AB) scans the genome to identify lesion-containing DNA. This process requires rapid binding and release of DNA; moreover, damage must be specifically recognized, and distinguished from native DNA, despite the fact that the relevant lesions induce widely different DNA structures. Once lesion-containing DNA has been located, it is stably bound by a dimeric form of UvrA within the AB complex (Stage 2). A major reorganization then occurs in which UvrA is lost from the ensemble, and concomitantly, UvrB becomes localized at the site of damage (Stage 3). Following these early stages, additional events lead to excision of the damage on one strand, and repair of the resulting single-stranded gap. Over the past few years, we have determined three structures of UvrA and the UvrA·UvrB complex. Our first structure of isolated UvrA revealed its overall architecture, its DNA binding surface, and the arrangement of its four-nucleotide binding sites. In the structure of the complete UvrA·UvrB damage sensor, a central UvrA dimer is flanked by two UvrB molecules, all linearly arrayed along a DNA path predicted by biochemical studies. DNA is predicted to bind to UvrA in the complex within a narrow and deep groove that is compatible with native duplex DNA only. In contrast, the shape of the corresponding surface in our prior structure of UvrA is wide and shallow, and appears compatible with various types of lesion-deformed DNA. These differences point to conformation switching between the two forms as a component of the genome-scanning phase of damage sensing. We also show that the highly conserved signature domain II of UvrA, which is adjacent to the proximal nucleotide-binding site, mediates a critical nexus of contacts to UvrB and to DNA. Moreover, in the novel UvrA conformer, the disposition of this domain is altered such that association with either UvrB or DNA is precluded. Concomitantly, nucleotide is uniquely absent from the proximal binding site. Thus, the signature domain II is implicated in an ATP-hydrolysis-dependent conformational change that detaches UvrA from both UvrB and DNA after initial damage recognition. The disposition and number of UvrB molecules in the AB complex, both unanticipated, suggest that once UvrA departs, UvrB localizes to the site of damage by helicase-mediated tracking along the DNA. Together these results permit a high-resolution model for the dynamics of early stages in NER.

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15

Delagoutte, Emmanuelle, Robert P. P. Fuchs i Elisabeth Bertrand-Burggraf. "The Isomerization of the UvrB–DNA Preincision Complex Couples the UvrB and UvrC Activities". Journal of Molecular Biology 320, nr 1 (czerwiec 2002): 73–84. http://dx.doi.org/10.1016/s0022-2836(02)00401-1.

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16

Lin, J. J., i A. Sancar. "Reconstitution of nucleotide excision nuclease with UvrA and UvrB proteins from Escherichia coli and UvrC protein from Bacillus subtilis." Journal of Biological Chemistry 265, nr 34 (grudzień 1990): 21337–41. http://dx.doi.org/10.1016/s0021-9258(17)45365-8.

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17

Alexandrovich, Alexander, Mark R. Sanderson, Geri F. Moolenaar, Nora Goosen i Andrew N. Lane. "NMR assignments and secondary structure of the UvrC binding domain of UvrB". FEBS Letters 451, nr 2 (21.05.1999): 181–85. http://dx.doi.org/10.1016/s0014-5793(99)00542-6.

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18

Sohi, Maninder, Alexander Alexandrovich, Geri Moolenaar, Rob Visse, Nora Goosen, Xavier Vernede, Juan C. Fontecilla-Camps, John Champness i Mark R. Sanderson. "Crystal structure of Escherichia coli UvrB C-terminal domain, and a model for UvrB-UvrC interaction". FEBS Letters 465, nr 2-3 (14.01.2000): 161–64. http://dx.doi.org/10.1016/s0014-5793(99)01690-7.

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19

Zou, Yue, Randall Walker, Heather Bassett, Nicholas E. Geacintov i Bennett Van Houten. "Formation of DNA Repair Intermediates and Incision by the ATP-dependent UvrB-UvrC Endonuclease". Journal of Biological Chemistry 272, nr 8 (21.02.1997): 4820–27. http://dx.doi.org/10.1074/jbc.272.8.4820.

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20

Tang, Moon Shong, James R. Pierce, Richard P. Doisy, Michael E. Nazimiec i Michael C. MacLeod. "Differences and similarities in the repair of two benzo[a]pyrenediol epoxide isomer-induced DNA adducts by uvrA, uvrB, and uvrC gene products". Biochemistry 31, nr 36 (wrzesień 1992): 8429–36. http://dx.doi.org/10.1021/bi00151a006.

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21

Silva, Rebekah M. B., Michael A. Grodick i Jacqueline K. Barton. "UvrC Coordinates an O2-Sensitive [4Fe4S] Cofactor". Journal of the American Chemical Society 142, nr 25 (29.05.2020): 10964–77. http://dx.doi.org/10.1021/jacs.0c01671.

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Hughes, Craig D., Hong Wang, Harshad Ghodke, Michelle Simons, Atif Towheed, Ye Peng, Bennett Van Houten i Neil M. Kad. "Real-time single-molecule imaging reveals a direct interaction between UvrC and UvrB on DNA tightropes". Nucleic Acids Research 41, nr 9 (19.03.2013): 4901–12. http://dx.doi.org/10.1093/nar/gkt177.

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Alexandrovich, Alexander, Mark R. Sanderson, Geri F. Moolenaar, Nora Goosen i Andrew N. Lane. "Corrigendum to: NMR assignments and secondary structure of the UvrC binding domain of UvrB (FEBS 22003)". FEBS Letters 456, nr 3 (11.08.1999): 417. http://dx.doi.org/10.1016/s0014-5793(99)00744-9.

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Badger, Julie L., i Virginia L. Miller. "Expression of Invasin and Motility Are Coordinately Regulated in Yersinia enterocolitica". Journal of Bacteriology 180, nr 4 (15.02.1998): 793–800. http://dx.doi.org/10.1128/jb.180.4.793-800.1998.

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ABSTRACT The Yersinia enterocolitica inv gene encodes the primary invasion factor invasin, which has been previously shown to be critical in the initial stages of infection. The expression ofinv is influenced by growth phase and temperature and is maximal during late exponential-early stationary phase at 23°C. In addition, motility of Y. enterocolitica is regulated by temperature. Y. enterocolitica cells are motile when grown at lower temperatures (30°C or below), while bacteria grown at 37°C are nonmotile. This study was initiated to determine the molecular basis for the temperature regulation of inv expression. Two mutants were isolated that both showed a significant decrease in invasin expression but are hypermotile when grown at 23°C. The first mutant (JB1A8v) was a result of a random mTn5Km insertion into the uvrC gene. The uvrC mutant JB1A8v demonstrated a significant decrease in inv and an increase in fleB (encodes flagellin) expression. These results suggest that expression of inv and flagellin genes is coordinated at the level of transcription. The second regulatory mutant, JB16v, was a result of a targeted insertion into a locus similar to sspA which in E. coli encodes a stationary-phase regulator. The E. coli sspA gene was cloned and assayed for complementation in both of the regulatory mutants. It was determined that E. coli sspA restored invasin expression in both the uvrC mutant and thesspA mutant. In addition, the complementing clone decreased flagellin levels in these mutants.

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Million-Weaver, Samuel, Ariana N. Samadpour, Daniela A. Moreno-Habel, Patrick Nugent, Mitchell J. Brittnacher, Eli Weiss, Hillary S. Hayden, Samuel I. Miller, Ivan Liachko i Houra Merrikh. "An underlying mechanism for the increased mutagenesis of lagging-strand genes inBacillus subtilis". Proceedings of the National Academy of Sciences 112, nr 10 (23.02.2015): E1096—E1105. http://dx.doi.org/10.1073/pnas.1416651112.

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We previously reported that lagging-strand genes accumulate mutations faster than those encoded on the leading strand inBacillus subtilis. Although we proposed that orientation-specific encounters between replication and transcription underlie this phenomenon, the mechanism leading to the increased mutagenesis of lagging-strand genes remained unknown. Here, we report that the transcription-dependent and orientation-specific differences in mutation rates of genes require theB. subtilisY-family polymerase, PolY1 (yqjH). We find that without PolY1, association of the replicative helicase, DnaC, and the recombination protein, RecA, with lagging-strand genes increases in a transcription-dependent manner. These data suggest that PolY1 promotes efficient replisome progression through lagging-strand genes, thereby reducing potentially detrimental breaks and single-stranded DNA at these loci. Y-family polymerases can alleviate potential obstacles to replisome progression by facilitating DNA lesion bypass, extension of D-loops, or excision repair. We find that the nucleotide excision repair (NER) proteins UvrA, UvrB, and UvrC, but not RecA, are required for transcription-dependent asymmetry in mutation rates of genes in the two orientations. Furthermore, we find that the transcription-coupling repair factor Mfd functions in the same pathway as PolY1 and is also required for increased mutagenesis of lagging-strand genes. Experimental and SNP analyses ofB. subtilisgenomes show mutational footprints consistent with these findings. We propose that the interplay between replication and transcription increases lesion susceptibility of, specifically, lagging-strand genes, activating an Mfd-dependent error-prone NER mechanism. We propose that this process, at least partially, underlies the accelerated evolution of lagging-strand genes.

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Skorvaga, Milan, Karsten Theis, Bhaskar S. Mandavilli, Caroline Kisker i Bennett Van Houten. "The β-Hairpin Motif of UvrB Is Essential for DNA Binding, Damage Processing, and UvrC-mediated Incisions". Journal of Biological Chemistry 277, nr 2 (30.10.2001): 1553–59. http://dx.doi.org/10.1074/jbc.m108847200.

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WALTERS, R. G., H. O. WILBRAHAM, P. STRIKE i J. W. FORSTER. "A Transposon Insertion in the Escherichia coli uvrC Gene; UvrC Protein is Absolutely Required for the Incision Step in Excision Repair". Microbiology 134, nr 2 (1.02.1988): 403–12. http://dx.doi.org/10.1099/00221287-134-2-403.

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Lagerbäck, Pernilla, i Karin Carlson. "Amino Acid Residues in the GIY-YIG Endonuclease II of Phage T4 Affecting Sequence Recognition and Binding as Well as Catalysis". Journal of Bacteriology 190, nr 16 (6.06.2008): 5533–44. http://dx.doi.org/10.1128/jb.00094-08.

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ABSTRACT Phage T4 endonuclease II (EndoII), a GIY-YIG endonuclease lacking a carboxy-terminal DNA-binding domain, was subjected to site-directed mutagenesis to investigate roles of individual amino acids in substrate recognition, binding, and catalysis. The structure of EndoII was modeled on that of UvrC. We found catalytic roles for residues in the putative catalytic surface (G49, R57, E118, and N130) similar to those described for I-TevI and UvrC; in addition, these residues were found to be important for substrate recognition and binding. The conserved glycine (G49) and arginine (R57) were essential for normal sequence recognition. Our results are in agreement with a role for these residues in forming the DNA-binding surface and exposing the substrate scissile bond at the active site. The conserved asparagine (N130) and an adjacent proline (P127) likely contribute to positioning the catalytic domain correctly. Enzymes in the EndoII subfamily of GIY-YIG endonucleases share a strongly conserved middle region (MR, residues 72 to 93, likely helical and possibly substituting for heterologous helices in I-TevI and UvrC) and a less strongly conserved N-terminal region (residues 12 to 24). Most of the conserved residues in these two regions appeared to contribute to binding strength without affecting the mode of substrate binding at the catalytic surface. EndoII K76, part of a conserved NUMOD3 DNA-binding motif of homing endonucleases found to overlap the MR, affected both sequence recognition and catalysis, suggesting a more direct involvement in positioning the substrate. Our data thus suggest roles for the MR and residues conserved in GIY-YIG enzymes in recognizing and binding the substrate.

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29

Forster, John W., i Peter Strike. "Organisation and control of the Escherichia coli uvrC gene". Gene 35, nr 1-2 (1985): 71–82. http://dx.doi.org/10.1016/0378-1119(85)90159-3.

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Orren, D. K., i A. Sancar. "The (A)BC excinuclease of Escherichia coli has only the UvrB and UvrC subunits in the incision complex." Proceedings of the National Academy of Sciences 86, nr 14 (1.07.1989): 5237–41. http://dx.doi.org/10.1073/pnas.86.14.5237.

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Moolenaar, Geri F., Kees L. M. C. Franken, Pieter van de Putte i Nora Goosen. "Function of the homologous regions of the Escherichia coli DNA excision repair proteins UvrB and UvrC in stabilization of the UvrBC–DNA complex and in 3′-incision". Mutation Research/DNA Repair 385, nr 3 (grudzień 1997): 195–203. http://dx.doi.org/10.1016/s0921-8777(97)00042-6.

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HOEIJMAKERS, J. H. J. "How Relevant is the Escherichia coli UvrABC Model for Excision Repair in Eukaryotes?" Journal of Cell Science 100, nr 4 (1.12.1991): 687–91. http://dx.doi.org/10.1242/jcs.100.4.687.

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Knowledge about the DNA excision repair system is increasing rapidly. A detailed model for this process in Escherichia coli has emerged in which a lesion in the DNA is first recognized by the UvrA2B helicase complex. Subsequently, UvrC mediates incision on both sites of the DNA injury. Finally, the concerted action of helicase II (UvrD), polymerase and ligase takes care of removal of the damage-containing oligonucleotide, DNA resynthesis and sealing of the residual nick. In the eukaryotes, yeast and mammals a total of 10 excision repair genes have been analysed thus far. However, little is still known about the molecular mechanism of this repair reaction. Amino acid sequence comparison suggests that at least three DNA helicases operate in eukaryotic nucleotide excision. In addition, a striking sequence conservation is noted between human and yeast repair proteins. But no eukaryotic homologs of the UvrABC proteins have been identified. In this Commentary the parallels and differences between the prokaryotic and eukaryotic excision repair pathways are weighed in an attempt to assess the relevance of the E. coli model for the eukaryotic system.

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33

Badger, Julie L., Briana M. Young, Andrew J. Darwin i Virginia L. Miller. "Yersinia enterocolitica ClpB Affects Levels of Invasin and Motility". Journal of Bacteriology 182, nr 19 (1.10.2000): 5563–71. http://dx.doi.org/10.1128/jb.182.19.5563-5571.2000.

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ABSTRACT Expression of the Yersinia enterocolitica inv gene is dependent on growth phase and temperature. inv is maximally expressed at 23°C in late-exponential- to early-stationary-phase cultures. We previously reported the isolation of a Y. enterocolitica mutant (JB1A8v) that shows a decrease in invasin levels yet is hypermotile when grown at 23°C. JB1A8v has a transposon insertion within uvrC. Described here is the isolation and characterization of a clone that suppresses these mutant phenotypes of the uvrC mutant JB1A8v. This suppressing clone encodes ClpB (a Clp ATPase homologue). The Y. enterocolitica ClpB homologue is 30 to 40% identical to the ClpB proteins from various bacteria but is 80% identical to one of the two ClpB homologues ofYersinia pestis. AclpB::TnMax2 insertion mutant (JB69Qv) was constructed and determined to be deficient in invasin production and nonmotile when grown at 23°C. Analysis ofinv and fleB (flagellin gene) transcript levels in JB69Qv suggested that ClpB has both transcriptional and posttranscriptional effects. In contrast, a clpB null mutant, BY1v, had no effect on invasin levels or motility. A model accounting for these observations is presented.

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Lage, Claudia, Silvia R. F. Gonçalves, Luciana L. Souza, Marcelo de Pádula i Alvaro C. Leitão. "Differential survival of Escherichia coli uvrA, uvrB, and uvrC mutants to psoralen plus UV-A (PUVA): Evidence for uncoupled action of nucleotide excision repair to process DNA adducts". Journal of Photochemistry and Photobiology B: Biology 98, nr 1 (styczeń 2010): 40–47. http://dx.doi.org/10.1016/j.jphotobiol.2009.11.001.

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Takahashi, Masayuki, Elisabeth Bertrand-Burggraf, Robert P. P. Fuchs i Bengt Nordén. "Structure of UvrABC excinuclease-UV-damaged DNA complexes studied by flow linear dichroism DNA curved by UvrB and UvrC". FEBS Letters 314, nr 1 (7.12.1992): 10–12. http://dx.doi.org/10.1016/0014-5793(92)81448-u.

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Stark, T., i R. E. Moses. "Interaction of the LexA repressor and the uvrC regulatory region". FEBS Letters 258, nr 1 (20.11.1989): 39–41. http://dx.doi.org/10.1016/0014-5793(89)81610-2.

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Register, Karen B., William D. Boatwright, Karen M. Gesy, Tyler C. Thacker i Murray D. Jelinski. "Mistaken identity of an open reading frame proposed for PCR-based identification of Mycoplasma bovis and the effect of polymorphisms and insertions on assay performance". Journal of Veterinary Diagnostic Investigation 30, nr 4 (29.03.2018): 637–41. http://dx.doi.org/10.1177/1040638718764799.

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Mycoplasma bovis is an important cause of disease in cattle and bison. Because the bacterium requires specialized growth conditions, many diagnostic laboratories routinely use PCR to replace or complement conventional isolation and identification methods. A frequently used target of such assays is the uvrC gene, which has been shown to be highly conserved among isolates. We discovered that a previously described PCR putatively targeting the uvrC gene amplifies a fragment from an adjacent gene predicted to encode a lipoprotein. Comparison of the lipoprotein gene sequence from 211 isolates revealed several single nucleotide polymorphisms, 1 of which falls within a primer-binding sequence. Additionally, 3 isolates from this group were found to have a 1,658-bp transposase gene insertion within the amplified region that leads to a false-negative result. The insertion was not detected in a further 164 isolates. We found no evidence that the nucleotide substitution within the primer-binding region affects the assay sensitivity, performance, or limit of detection. Nonetheless, laboratories utilizing this method for identification of M. bovis should be aware that the region amplified may be prone to nucleotide substitutions and/or insertions relative to the sequence used for its design and that occasional false-negative results may be obtained.

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38

Viswanathan, Mohan, Anne Lanjuin i Susan T. Lovett. "Identification of RNase T as a High-Copy Suppressor of the UV Sensitivity Associated With Single-Strand DNA Exonuclease Deficiency in Escherichia coli". Genetics 151, nr 3 (1.03.1999): 929–34. http://dx.doi.org/10.1093/genetics/151.3.929.

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Abstract There are three known single-strand DNA-specific exonucleases in Escherichia coli: RecJ, exonuclease I (ExoI), and exonuclease VII (ExoVII). E. coli that are deficient in all three exonucleases are abnormally sensitive to UV irradiation, most likely because of their inability to repair lesions that block replication. We have performed an iterative screen to uncover genes capable of ameliorating the UV repair defect of xonA (ExoI-) xseA (ExoVII-) recJ triple mutants. In this screen, exonuclease-deficient cells were transformed with a high-copy E. coli genomic library and then irradiated; plasmids harvested from surviving cells were used to seed subsequent rounds of transformation and selection. After several rounds of selection, multiple plasmids containing the rnt gene, which encodes RNase T, were found. An rnt plasmid increased the UV resistance of a xonA xseA recJ mutant and uvrA and uvrC mutants; however, it did not alter the survival of xseA recJ or recA mutants. RNase T also has amino acid sequence similarity to other 3′ DNA exonucleases, including ExoI. These results suggest that RNase T may possess a 3′ DNase activity capable of substituting for ExoI in the recombinational repair of UV-induced lesions.

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39

Silva, Rebekah M. B., Andy Zhou, Michael A. Grodick i Jacqueline K. Barton. "DNA-Mediated Redox Signaling in Bacterial Nucleotide Excision Repair by UvrC". Biophysical Journal 110, nr 3 (luty 2016): 62a—63a. http://dx.doi.org/10.1016/j.bpj.2015.11.403.

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Salem, Amir M. H., Toshiaki Nakano, Minako Takuwa, Nagisa Matoba, Tomohiro Tsuboi, Hiroaki Terato, Kazuo Yamamoto, Masami Yamada, Takehiko Nohmi i Hiroshi Ide. "Genetic Analysis of Repair and Damage Tolerance Mechanisms for DNA-Protein Cross-Links in Escherichia coli". Journal of Bacteriology 191, nr 18 (17.07.2009): 5657–68. http://dx.doi.org/10.1128/jb.00417-09.

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ABSTRACT DNA-protein cross-links (DPCs) are unique among DNA lesions in their unusually bulky nature. We have recently shown that nucleotide excision repair (NER) and RecBCD-dependent homologous recombination (HR) collaboratively alleviate the lethal effect of DPCs in Escherichia coli. In this study, to gain further insight into the damage-processing mechanism for DPCs, we assessed the sensitivities of a panel of repair-deficient E. coli mutants to DPC-inducing agents, including formaldehyde (FA) and 5-azacytidine (azaC). We show here that the damage tolerance mechanism involving HR and subsequent replication restart (RR) provides the most effective means of cell survival against DPCs. Translesion synthesis does not serve as an alternative damage tolerance mechanism for DPCs in cell survival. Elimination of DPCs from the genome relies primarily on NER, which provides a second and moderately effective means of cell survival against DPCs. Interestingly, Cho rather than UvrC seems to be an effective nuclease for the NER of DPCs. Together with the genes responsible for HR, RR, and NER, the mutation of genes involved in several aspects of DNA repair and transactions, such as recQ, xth nfo, dksA, and topA, rendered cells slightly but significantly sensitive to FA but not azaC, possibly reflecting the complexity of DPCs or cryptic lesions induced by FA. UvrD may have an additional role outside NER, since the uvrD mutation conferred a slight azaC sensitivity on cells. Finally, DNA glycosylases mitigate azaC toxicity, independently of the repair of DPCs, presumably by removing 5-azacytosine or its degradation product from the chromosome.

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41

Tang, Moon-shong, Michael Nazimiec, Xiangcang Ye, Ganesh H. Iyer, Jamie Eveleigh, Yi Zheng, Wenjing Zhou i Yen-Yee Tang. "Two Forms of UvrC Protein with Different Double-stranded DNA Binding Affinities". Journal of Biological Chemistry 276, nr 6 (30.10.2000): 3904–10. http://dx.doi.org/10.1074/jbc.m008538200.

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Rahden-Staroń, I., M. Szumiło i P. Ziemkiewicz. "The effects of captan and captafol on different bacterial strains and on c-mitosis in V79 Chinese hamster fibroblasts." Acta Biochimica Polonica 41, nr 1 (31.03.1994): 45–55. http://dx.doi.org/10.18388/abp.1994_4773.

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The mutagenic activity of captan and captafol was tested using Ames strains and strains showing an SOS response. Captafol was mutagenic in S. typhimurium strain TA102 (uvr+) and captan in strain TA104 (uvrB). Both captan and captafol elicit damages in DNA recognized by correndonuclease II, as shown by the repair test, and induced the SOS repair system in E. coli PQ37 (uvrA) strain. Only captafol induced the SOS system in PQ35 (uvr+). The lack of induction of beta-galactosidase at nonpermissive temperature in E. coli MD332 (dnaCs uvrA) strain showed that neither chemical was able to produce DNA breaks. In V79 Chinese hamster fibroblasts higher induction of c-mitosis by captafol than by captan (22% and 15% over the control, respectively) was accompanied by a higher decrease in nonprotein sulfhydryl groups, mainly GSH (41% and 77%, respectively). The content of protein sulfhydryl groups was decreased by either fungicide to a similar extent.

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43

Wei, Yan, Jian-Ming Lee, Dana R. Smulski i Robert A. LaRossa. "Global Impact of sdiA Amplification Revealed by Comprehensive Gene Expression Profiling of Escherichia coli". Journal of Bacteriology 183, nr 7 (1.04.2001): 2265–72. http://dx.doi.org/10.1128/jb.183.7.2265-2272.2001.

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ABSTRACT In Escherichia coli the amplification ofsdiA, a positive activator of ftsQAZ, genes that are essential for septation, results in mitomycin C resistance. To help us understand this resistance phenotype, genes whose expression was altered by increased sdiA dosage were identified using a DNA microarray-based, comprehensive transcript profiling method. The expression of 62 genes was reduced by more than threefold; of these, 41 are involved in motility and chemotaxis. Moreover, the expression of 75 genes, 36 of which had been previously characterized, was elevated at least threefold. As expected, increased sdiA dosage led to significantly elevated sdiA and ′ddlB-ftsQAZ-lpxC operon expression. Transcription of two genes, uvrY and uvrC, located downstream ofsdiA and oriented in the same direction, was elevated about 10-fold, although the intervening gene, yecF, of opposite polarity was unaffected by increased sdiA dosage. Three genes (mioC and gidAB) flanking the replication origin, oriC, were transcribed more often whensdiA dosage was high, as were 12 genes within 1 min of a terminus of replication, terB. Transcription of theacrABDEF genes, mapping in three widely spaced loci, was elevated significantly, while several genes involved in DNA repair and replication (e.g., nei, recN, mioC, and mcrC) were moderately elevated in expression. Such global analysis provides a link between septation and the response to DNA-damaging agents.

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44

Lin, J. J., i A. Sancar. "The C-terminal half of UvrC protein is sufficient to reconstitute (A)BC excinuclease." Proceedings of the National Academy of Sciences 88, nr 15 (1.08.1991): 6824–28. http://dx.doi.org/10.1073/pnas.88.15.6824.

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Bichara, M., i R. P. Fuchs. "uvrC gene function has no specific role in repair of N-2-aminofluorene adducts." Journal of Bacteriology 169, nr 1 (1987): 423–26. http://dx.doi.org/10.1128/jb.169.1.423-426.1987.

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Singh, S., G. E. Folkers, A. M. J. J. Bonvin, R. Boelens, R. Wechselberger, A. Niztayev i R. Kaptein. "Solution structure and DNA-binding properties of the C-terminal domain of UvrC from E.coli". EMBO Journal 21, nr 22 (15.11.2002): 6257–66. http://dx.doi.org/10.1093/emboj/cdf627.

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THOMAS, A. "Conservation of the uvrC gene sequence in Mycoplasma bovis and its use in routine PCR diagnosis". Veterinary Journal 168, nr 1 (lipiec 2004): 100–102. http://dx.doi.org/10.1016/s1090-0233(03)00186-2.

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Verhoeven, Esther E. A., Marian van Kesteren, Geri F. Moolenaar, Rob Visse i Nora Goosen. "Catalytic Sites for 3′ and 5′ Incision ofEscherichia coliNucleotide Excision Repair Are Both Located in UvrC". Journal of Biological Chemistry 275, nr 7 (18.02.2000): 5120–23. http://dx.doi.org/10.1074/jbc.275.7.5120.

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Forster, John W., i Peter Strike. "Analysis of the regulatory elements of the Escherichia coli uvrC gene by construction of operon fusions". Molecular and General Genetics MGG 211, nr 3 (marzec 1988): 531–37. http://dx.doi.org/10.1007/bf00425712.

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Moolenaar, Geri F., Kees L. M. C. Franken, Doesjka M. Dijkstra, Jane E. Thomas-Oates, Rob Visse, Pieter van de Putte i Nora Goosen. "The C-terminal Region of the UvrB Protein ofEscherichia coliContains an Important Determinant for UvrC Binding to the Preincision Complex but Not the Catalytic Site for 3′-Incision". Journal of Biological Chemistry 270, nr 51 (22.12.1995): 30508–15. http://dx.doi.org/10.1074/jbc.270.51.30508.

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