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• W2085703356 abstract "The Escherichia coli Uvr(A)BC endonuclease (Uvr(A)BC) initiates nucleotide excision repair of a large variety of DNA damages. The damage recognition and incision steps by the Uvr(A)BC is a complex process utilizing an ATP-dependent DNA helix-tracking activity associated with the UvrA2B1 complex. The latter activity leads to the generation of highly positively supercoiled DNA in the presence of E. coli topoisomerase I in vitro. Such highly positively supercoiled DNA, containing ultraviolet irradiation-induced photoproducts (uvDNA), is resistant to the incision by Uvr(A)BC, whereas the negatively supercoiled and relaxed forms of the uvDNA are effectively incised. The E. coli gyrase can contribute to the above reaction by abolishing the accumulation of highly positively supercoiled uvDNA thereby restoring Uvr(A)BC-catalyzed incision. Eukaryotic (calf thymus) topoisomerase I is able to substitute for gyrase in restoring this Uvr(A)BC-mediated incision reaction. The inability of Uvr(A)BC to incise highly positively supercoiled uvDNA results from the failure of the formation of UvrAB-dependent obligatory intermediates associated with the DNA conformational change. In contrast to Uvr(A)BC, the Micrococcus luteus UV endonuclease efficiently incises uvDNA regardless of its topological state. The in vitro topodynamic system proposed in this study may provide a simple model for studying a topological aspect of nucleotide excision repair and its interaction with other DNA topology-related processes in E. coli. The Escherichia coli Uvr(A)BC endonuclease (Uvr(A)BC) initiates nucleotide excision repair of a large variety of DNA damages. The damage recognition and incision steps by the Uvr(A)BC is a complex process utilizing an ATP-dependent DNA helix-tracking activity associated with the UvrA2B1 complex. The latter activity leads to the generation of highly positively supercoiled DNA in the presence of E. coli topoisomerase I in vitro. Such highly positively supercoiled DNA, containing ultraviolet irradiation-induced photoproducts (uvDNA), is resistant to the incision by Uvr(A)BC, whereas the negatively supercoiled and relaxed forms of the uvDNA are effectively incised. The E. coli gyrase can contribute to the above reaction by abolishing the accumulation of highly positively supercoiled uvDNA thereby restoring Uvr(A)BC-catalyzed incision. Eukaryotic (calf thymus) topoisomerase I is able to substitute for gyrase in restoring this Uvr(A)BC-mediated incision reaction. The inability of Uvr(A)BC to incise highly positively supercoiled uvDNA results from the failure of the formation of UvrAB-dependent obligatory intermediates associated with the DNA conformational change. In contrast to Uvr(A)BC, the Micrococcus luteus UV endonuclease efficiently incises uvDNA regardless of its topological state. The in vitro topodynamic system proposed in this study may provide a simple model for studying a topological aspect of nucleotide excision repair and its interaction with other DNA topology-related processes in E. coli. INTRODUCTIONThe Uvr(A)BC endonuclease from Escherichia coli consists of an ensemble of the uvrA, uvrB, and uvrC gene products. They act in a sequential manner to produce dual incision of damaged DNA strand at the fourth (fifth) phosphodiester bond 3′ and the eighth phosphodiester bond 5′ to the damaged site, respectively (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 2Lin J.-J. Sancar A. Mol. Microbiol. 1992; 6: 2219-2224Crossref PubMed Scopus (91) Google Scholar, 3Van Houten B. Microbiol. Rev. 1990; 54: 18-51Crossref PubMed Google Scholar). The NER 1The abbreviations used are: NERnucleotide excision repairUvr(A)BCUvr(A)BC endonuclease; M. luteus UV endo, M. luteus UV endonuclease; topo I, topoisomerase of type IUVultraviolet (254 nm) irradiationuvDNAUV-irradiated DNAccDNAcovalently closed circular DNABSAbovine serum albuminDTTdithiothreitolMOPS4-morpholinepropanesulfonic acid. process is completed in vitro by the subsequent action of DNA helicase II (UvrD), DNA polymerase I, dNTPs, and ligase (4Caron P.R. Kushner S.R. Grossman L. Proc. Natl. Acad. Sci. U. S. A. 1985; 82: 4925-4929Crossref PubMed Scopus (136) Google Scholar, 5Orren D.K. Selby C.R. Hearst J.E. Sancar A. J. Biol. Chem. 1992; 267: 780-788Abstract Full Text PDF PubMed Google Scholar). The Uvr(A)BC is able to act on a very broad spectrum of DNA damage (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 2Lin J.-J. Sancar A. Mol. Microbiol. 1992; 6: 2219-2224Crossref PubMed Scopus (91) Google Scholar, 3Van Houten B. Microbiol. Rev. 1990; 54: 18-51Crossref PubMed Google Scholar, 6Lloyd R.S. Van Houten B. Vos J.-M.H. DNA Repair Mechanisms: Impact on Human Diseases and Cancer. R. G. Landes Co., Austin1995: 25-66Google Scholar). In the damage recognition and incision steps, an intricate ATP hydrolysis-coupled process is employed rather than direct damage binding-incision utilized by most of the damage-specific repair enzymes (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 2Lin J.-J. Sancar A. Mol. Microbiol. 1992; 6: 2219-2224Crossref PubMed Scopus (91) Google Scholar, 3Van Houten B. Microbiol. Rev. 1990; 54: 18-51Crossref PubMed Google Scholar, 6Lloyd R.S. Van Houten B. Vos J.-M.H. DNA Repair Mechanisms: Impact on Human Diseases and Cancer. R. G. Landes Co., Austin1995: 25-66Google Scholar). In particular, a DNA helix-tracking activity of UvrA2B1 complex is engaged in search and/or prepriming of damage by Uvr(A)BC (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 7Koo H.-S. Claassen L. Grossman L. Liu L.F. Proc. Natl. Acad. Sci. U. S. A. 1991; 88: 1212-1216Crossref PubMed Scopus (67) Google Scholar). Such DNA helix-tracking activity generates domains of positive and negative supercoils ahead and behind moving complex, respectively (7Koo H.-S. Claassen L. Grossman L. Liu L.F. Proc. Natl. Acad. Sci. U. S. A. 1991; 88: 1212-1216Crossref PubMed Scopus (67) Google Scholar, 8Wu H.-Y. Shyy S. Wang J.C. Liu L.F. Cell. 1988; 53: 433-440Abstract Full Text PDF PubMed Scopus (538) Google Scholar). The differential accumulation of either positive or negative supercoils, which can be achieved in the presence of “anchoring” entities (9Wang J.C. Lynch A.S. Curr. Opinion Genet. Dev. 1993; 3: 764-768Crossref PubMed Scopus (110) Google Scholar, 10Wang, J. C., (1992) Transcriptional Regulation, (McNight, S. L., Yamamoto, K. R., eds), Vol. 2, pp. 1253‒1269, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY.Google Scholar), could potentially affect the tracking activity of the UvrA2B1 complex and, hence, influence the DNA repair process. In the cell, the topoisomerase activities are involved in preventing such accumulation and maintaining the proper level of DNA superhelicity (8Wu H.-Y. Shyy S. Wang J.C. Liu L.F. Cell. 1988; 53: 433-440Abstract Full Text PDF PubMed Scopus (538) Google Scholar, 11Gellert M. Annu. Rev. Biochem. 1981; 50: 879-910Crossref PubMed Scopus (855) Google Scholar, 12Wang J.C. Annu. Rev. Biochem. 1985; 54: 665-698Crossref PubMed Scopus (1635) Google Scholar, 13Liu L.F. Wang J. Proc. Natl. Acad. Sci. U. S. A. 1987; 84: 7024-7027Crossref PubMed Scopus (1487) Google Scholar). It was found that topo I and gyrase mutations as well as gyrase inhibitors (novobiocin and nalidixic acid) increase sensitivity of E. coli cells to the killing effects of UV irradiation, affect to different degrees the amount of UV-stimulated repair synthesis, and inhibit recovery of UV-irradiated nonreplicative λ phage (14Crumplin G.C. Carcinogenesis. 1981; 2: 157-160Crossref PubMed Scopus (32) Google Scholar, 15Sternglanz R. DiNardo S. Voelkel K.A. Nishimura Y. Hirota Y. Becherer K. Zumstein L. Wang J.C. Proc. Natl. Acad. Sci. U. S. A. 1981; 78: 2747-2751Crossref PubMed Scopus (194) Google Scholar, 16Purdy M.A. Yeilding L. Antimicrob. Agents Chemother. 1976; 10: 182-184Crossref PubMed Scopus (2) Google Scholar, 17Simon T. Masker W.E. Hanawalt P.C. Biochim. Biophys. Acta. 1974; 349: 271-274Crossref PubMed Scopus (21) Google Scholar, 18Hays J.B. Boehmer S. Proc. Natl. Acad. Sci. U. S. A. 1978; 80: 4125-4129Crossref Scopus (38) Google Scholar). These observations give a hint of the existence of the topological aspect of NER in vivo. However, the effect of damaged DNA topological state on and involvement of topoisomerases in NER in E. coli have received so far very limited biochemical characterization (19Friedberg E.C. Walker G.C. Siede W. DNA Repair and Mutagenesis. ASM Press, Washington, D. C.1995: 218Google Scholar, 20Munn M. Rupp D. J. Biol. Chem. 1991; 266: 24748-24756Abstract Full Text PDF PubMed Google Scholar, 21Backendorf C. Olsthoorn R. van de Putte P. Nucleic Acids. Res. 1989; 17: 10337-10351Crossref PubMed Scopus (11) Google Scholar, 22Pedrini A.M. Ciarocchi G. Proc. Natl. Acad. Sci. U. S. A. 1983; 80: 1787-1791Crossref PubMed Scopus (26) Google Scholar). In this report, we addressed this question using the in vitro system including Uvr proteins and topoisomerases. This topodynamic (23Kozyavkin S. Slesarev A.I. Malkhosyan S.R. Panyutin I.G. Eur. J. Biochem. 1990; 191: 105-113Crossref PubMed Scopus (10) Google Scholar, 24Kovalsky O.I. Kozyavkin S.A. Slesarev A.I. Nucleic Acids Res. 1990; 18: 2801-2805Crossref PubMed Scopus (32) Google Scholar) system allows for the differential regulation of the uvDNA topological state. It was found that highly positively supercoiled uvDNA generated by UvrA2B1 helix-tracking activity in the presence of only E. coli topo I is not incised by Uvr(A)BC, whereas it is efficiently incised by Micrococcus luteus UV endo. The addition to this reaction mixture of enzymatic activities removing positive supercoils (E. coli gyrase or eukaryotic topo I) results in restoration of the incision of uvDNA by Uvr(A)BC. The inability of Uvr(A)BC to incise highly positively supercoiled uvDNA is due to the inhibition of UvrAB-dependent incision intermediates associated with the DNA substrate conformational change (25Oh E.Y. Grossman L. Nucleic Acids Res. 1986; 14: 8557-8571Crossref PubMed Scopus (46) Google Scholar). The results are discussed in terms of the influence of DNA topology on the process of Uvr(A)BC damage recognition and incision as well as in terms of the applicability of this in vitro topodynamic system for study of the topological aspect of NER and its interaction with other DNA topology-involved cellular processes.DISCUSSIONNER of damaged DNA can be accomplished in vitro by six highly purified E. coli proteins. The three components of Uvr(A)BC acting in a sequential and coordinated manner initiate repair by carrying out dual incision of the damaged strand. The incision step is a complex ATP-dependent process involving structural changes of protein and nucleoprotein intermediates. The combined action of UvrD (helicase II) and DNA polymerase I in the presence of dNTPs results in a displacement of postincision Uvr protein-incised fragment complex(es) and resynthesis of DNA. DNA ligase completes the repair by restoring the integrity of DNA (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 2Lin J.-J. Sancar A. Mol. Microbiol. 1992; 6: 2219-2224Crossref PubMed Scopus (91) Google Scholar). This in vitro system neither requires any of the known E. coli topoisomerases nor takes into account a potential influence of the DNA topology on NER process. However, the reconstituted NER system underrates the dynamic nature of DNA in vivo with respect to its topology. In particular, translocation-involved cellular processes, notably transcription and replication, generate domains of negative and positive supercoiling behind and ahead of a translocating complex (8Wu H.-Y. Shyy S. Wang J.C. Liu L.F. Cell. 1988; 53: 433-440Abstract Full Text PDF PubMed Scopus (538) Google Scholar, 9Wang J.C. Lynch A.S. Curr. Opinion Genet. Dev. 1993; 3: 764-768Crossref PubMed Scopus (110) Google Scholar, 10Wang, J. C., (1992) Transcriptional Regulation, (McNight, S. L., Yamamoto, K. R., eds), Vol. 2, pp. 1253‒1269, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY.Google Scholar, 13Liu L.F. Wang J. Proc. Natl. Acad. Sci. U. S. A. 1987; 84: 7024-7027Crossref PubMed Scopus (1487) Google Scholar). Although this differential supercoiling may not be persistent in an in vitro reconstituted system, the large protein-, nucleoprotein-, and membrane-involved in vivo macromolecular assemblies are able to function as “anchoring” structures preventing or slowing down the fusion of opposite supercoils (9Wang J.C. Lynch A.S. Curr. Opinion Genet. Dev. 1993; 3: 764-768Crossref PubMed Scopus (110) Google Scholar, 10Wang, J. C., (1992) Transcriptional Regulation, (McNight, S. L., Yamamoto, K. R., eds), Vol. 2, pp. 1253‒1269, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY.Google Scholar). Given that the incision step of Uvr(A)BC-dependent NER utilizes DNA helix-tracking activity and proceeds through DNA conformational changes resulting in DNA unwinding (25Oh E.Y. Grossman L. Nucleic Acids Res. 1986; 14: 8557-8571Crossref PubMed Scopus (46) Google Scholar), it is reasonable to expect that NER can be influenced by the topological waves of opposite supercoiling. This reasoning is strengthened by the phenomenon of transcription-coupled repair (37Melon I. Hanawalt P.C. Nature. 1981; 342: 95-98Crossref Scopus (463) Google Scholar, 38Selby C.P. Sancar A. Microbiol. Rev. 1994; 58: 317-329Crossref PubMed Google Scholar). The transcription and repair macromolecular assemblies seem to be in a physical association during this process. 4It was shown that the β-subunit of the E. coli RNA polymerase and UvrA protein can be reversibly cross-linked in vivo (C.-L. Lin, O. I. Kovalsky, and L. Grossman, manuscript in preparation). Furthermore, the Uvr(A)BC complex seems to preferentially operate downstream of the transcription machinery (39Ahn B. Grossman L. J. Biol. Chem. 1996; 271: 21453-21461Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar, 40Ahn B. Grossman L. J. Biol. Chem. 1996; 271: 21462-21470Abstract Full Text Full Text PDF PubMed Scopus (23) Google Scholar), that is, in the region of potential positive supercoiling. In supporting this suggestion, we found that highly positively supercoiled DNA, generated under conditions of supercoiling assay (7Koo H.-S. Claassen L. Grossman L. Liu L.F. Proc. Natl. Acad. Sci. U. S. A. 1991; 88: 1212-1216Crossref PubMed Scopus (67) Google Scholar), is resistant to the incision by Uvr(A)BC. Such DNA is refractory to two of the UvrAB-dependent functions thought to be associated with the formation of obligatory intermediates in the Uvr(A)BC-catalyzed incision (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar): (i) the robust stimulation of the UvrA2B1-associated ATPase is not observed and (ii) no stable damage-dependent nucleoprotein complexes are formed. It was found earlier that these obligatory intermediates are associated with the DNA conformational changes resulting in the decrease of a number of helical turns in a ccDNA (25Oh E.Y. Grossman L. Nucleic Acids Res. 1986; 14: 8557-8571Crossref PubMed Scopus (46) Google Scholar). Such a decrease should be compensated by an increase in the number of superhelical turns in order to maintain a constant linking number of ccDNA (32Wang J. Peck L.J. Becherer K. Cold Spring Harbor Symp. Quant. Biol. 1983; 47: 85-91Crossref PubMed Google Scholar). In cases of positively supercoiled DNA, this compensation would result in an unfavorable free energy change (41Frank-Kamenetskii M.D. Cozarelli N.R. Wang J.C. DNA Topology and Its Biological Effects. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY1990: 185-215Google Scholar). The energy input produced by the UvrAB-associated ATPase, which probably provides for power stroke during the above conformational change (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar), may not be sufficient to overcome that unfavorable free energy change. As a result, obligatory intermediates in this process are unable to form on highly positively supercoiled DNA. In cases of highly negatively supercoiled DNA, produced when gyrase substitutes for E. coli topo I in the supercoiling assay, a decrease in the number of helical turns should be energetically favorable (41Frank-Kamenetskii M.D. Cozarelli N.R. Wang J.C. DNA Topology and Its Biological Effects. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY1990: 185-215Google Scholar). Hence, the formation of intermediates in question should be facilitated. Consistently, this DNA was found to be efficiently incised by Uvr(A)BC.It was shown that in the absence of UvrB, UvrA protein recognizes damage by random diffusion mechanism, and its binding does not result in a significant DNA unwinding (25Oh E.Y. Grossman L. Nucleic Acids Res. 1986; 14: 8557-8571Crossref PubMed Scopus (46) Google Scholar, 30Mazur S.J. Grossman L. Biochemistry. 1991; 30: 4432-4443Crossref PubMed Scopus (83) Google Scholar). Consequently, the UvrA protein was able to recognize and bind damaged sites on highly positively supercoiled uvDNA. This further supports the earlier observations that affinity of UvrA for damage does not correlate with the efficiency of incision (42Bertrand-Burggraf E. Selby C.P. Hearst J.E. Sancar A. J. Mol. Biol. 1991; 219: 27-36Crossref PubMed Scopus (55) Google Scholar, 43Snowden A. Van Houten B. J. Mol. Biol. 1991; 220: 19-33Crossref PubMed Scopus (29) Google Scholar) and that UvrAB complex provides for a more productive DNA-binding intermediate (39Ahn B. Grossman L. J. Biol. Chem. 1996; 271: 21453-21461Abstract Full Text Full Text PDF PubMed Scopus (9) Google Scholar, 40Ahn B. Grossman L. J. Biol. Chem. 1996; 271: 21462-21470Abstract Full Text Full Text PDF PubMed Scopus (23) Google Scholar). Notably, M. luteus UV endo which by analogy with T4 phage UV endonuclease seems to directly recognize cyclobutane pyrimidine dimers and does not induce extensive DNA unwinding (28Grafstrom R.H. Park L. Grossman L. J. Biol. Chem. 1982; 257: 13465-13474Abstract Full Text PDF PubMed Google Scholar, 44Vassylyev D.G. Kashiwagi T. Mikami Y. Ariyoshi M. Iwai S. Ohtsuka E. Morikava K. Cell. 1995; 83: 773-782Abstract Full Text PDF PubMed Scopus (256) Google Scholar) efficiently incised uvDNA regardless of its topological state.The problem of incising highly positively supercoiled uvDNA by Uvr(A)BC is reminiscent of transcription and replication encountering accumulated positive supercoils (45Gartenberger M.R. Wang J.C. Proc. Natl. Acad. Sci. U. S. A. 1992; 89: 11461-11465Crossref PubMed Scopus (78) Google Scholar, 46Hiasa H. Marians K.J. J. Biol. Chem. 1994; 269: 16371-16375Abstract Full Text PDF PubMed Google Scholar, 47Hiasa H. Marians K.J. J. Biol. Chem. 1994; 269: 32655-32659Abstract Full Text PDF PubMed Google Scholar). E. coli possesses two major topoisomerases responsible for maintaining adequate superhelical stress: topo I removes negative supercoils whereas gyrase introduces negative supercoils. The presence of both activities in the supercoiling assay abolished accumulation of highly positively supercoiled uvDNA and restored incision by Uvr(A)BC. The eukaryotic (calf thymus) topo I, capable of removing positive supercoils, was able to substitute for gyrase in restoring Uvr(A)BC incision. Hence, the restoration of incision seems to take place namely due to prevention of the accumulation of positive supercoils. In support of the existence of similar topological problems in vivo, both E. coli gyrase and topo I are recruited in a damage-dependent manner (among other NER-related and seemingly unrelated proteins) to the inner membrane of the UV-irradiated cells as a part of SOS response. 5C.-L. Lin, O. I. Kovalsky, and L. Grossman, manuscript in preparation. These topoisomerases may be required to regulate DNA topology for optimum repair in such membrane-attached configuration.The topodynamic in vitro system described in this report may be a prototype for studying different aspects of the interrelation of NER and DNA topology. By using specific ccDNA templates, different combinations of topoisomerases, and other macromolecular entities in the system, it is feasible to gain insights into the interaction of NER and other DNA topology-involved cellular processes. INTRODUCTIONThe Uvr(A)BC endonuclease from Escherichia coli consists of an ensemble of the uvrA, uvrB, and uvrC gene products. They act in a sequential manner to produce dual incision of damaged DNA strand at the fourth (fifth) phosphodiester bond 3′ and the eighth phosphodiester bond 5′ to the damaged site, respectively (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 2Lin J.-J. Sancar A. Mol. Microbiol. 1992; 6: 2219-2224Crossref PubMed Scopus (91) Google Scholar, 3Van Houten B. Microbiol. Rev. 1990; 54: 18-51Crossref PubMed Google Scholar). The NER 1The abbreviations used are: NERnucleotide excision repairUvr(A)BCUvr(A)BC endonuclease; M. luteus UV endo, M. luteus UV endonuclease; topo I, topoisomerase of type IUVultraviolet (254 nm) irradiationuvDNAUV-irradiated DNAccDNAcovalently closed circular DNABSAbovine serum albuminDTTdithiothreitolMOPS4-morpholinepropanesulfonic acid. process is completed in vitro by the subsequent action of DNA helicase II (UvrD), DNA polymerase I, dNTPs, and ligase (4Caron P.R. Kushner S.R. Grossman L. Proc. Natl. Acad. Sci. U. S. A. 1985; 82: 4925-4929Crossref PubMed Scopus (136) Google Scholar, 5Orren D.K. Selby C.R. Hearst J.E. Sancar A. J. Biol. Chem. 1992; 267: 780-788Abstract Full Text PDF PubMed Google Scholar). The Uvr(A)BC is able to act on a very broad spectrum of DNA damage (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 2Lin J.-J. Sancar A. Mol. Microbiol. 1992; 6: 2219-2224Crossref PubMed Scopus (91) Google Scholar, 3Van Houten B. Microbiol. Rev. 1990; 54: 18-51Crossref PubMed Google Scholar, 6Lloyd R.S. Van Houten B. Vos J.-M.H. DNA Repair Mechanisms: Impact on Human Diseases and Cancer. R. G. Landes Co., Austin1995: 25-66Google Scholar). In the damage recognition and incision steps, an intricate ATP hydrolysis-coupled process is employed rather than direct damage binding-incision utilized by most of the damage-specific repair enzymes (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 2Lin J.-J. Sancar A. Mol. Microbiol. 1992; 6: 2219-2224Crossref PubMed Scopus (91) Google Scholar, 3Van Houten B. Microbiol. Rev. 1990; 54: 18-51Crossref PubMed Google Scholar, 6Lloyd R.S. Van Houten B. Vos J.-M.H. DNA Repair Mechanisms: Impact on Human Diseases and Cancer. R. G. Landes Co., Austin1995: 25-66Google Scholar). In particular, a DNA helix-tracking activity of UvrA2B1 complex is engaged in search and/or prepriming of damage by Uvr(A)BC (1Grossman L. Thiagalingam S. J. Biol. Chem. 1993; 268: 16871-16874Abstract Full Text PDF PubMed Google Scholar, 7Koo H.-S. Claassen L. Grossman L. Liu L.F. Proc. Natl. Acad. Sci. U. S. A. 1991; 88: 1212-1216Crossref PubMed Scopus (67) Google Scholar). Such DNA helix-tracking activity generates domains of positive and negative supercoils ahead and behind moving complex, respectively (7Koo H.-S. Claassen L. Grossman L. Liu L.F. Proc. Natl. Acad. Sci. U. S. A. 1991; 88: 1212-1216Crossref PubMed Scopus (67) Google Scholar, 8Wu H.-Y. Shyy S. Wang J.C. Liu L.F. Cell. 1988; 53: 433-440Abstract Full Text PDF PubMed Scopus (538) Google Scholar). The differential accumulation of either positive or negative supercoils, which can be achieved in the presence of “anchoring” entities (9Wang J.C. Lynch A.S. Curr. Opinion Genet. Dev. 1993; 3: 764-768Crossref PubMed Scopus (110) Google Scholar, 10Wang, J. C., (1992) Transcriptional Regulation, (McNight, S. L., Yamamoto, K. R., eds), Vol. 2, pp. 1253‒1269, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY.Google Scholar), could potentially affect the tracking activity of the UvrA2B1 complex and, hence, influence the DNA repair process. In the cell, the topoisomerase activities are involved in preventing such accumulation and maintaining the proper level of DNA superhelicity (8Wu H.-Y. Shyy S. Wang J.C. Liu L.F. Cell. 1988; 53: 433-440Abstract Full Text PDF PubMed Scopus (538) Google Scholar, 11Gellert M. Annu. Rev. Biochem. 1981; 50: 879-910Crossref PubMed Scopus (855) Google Scholar, 12Wang J.C. Annu. Rev. Biochem. 1985; 54: 665-698Crossref PubMed Scopus (1635) Google Scholar, 13Liu L.F. Wang J. Proc. Natl. Acad. Sci. U. S. A. 1987; 84: 7024-7027Crossref PubMed Scopus (1487) Google Scholar). It was found that topo I and gyrase mutations as well as gyrase inhibitors (novobiocin and nalidixic acid) increase sensitivity of E. coli cells to the killing effects of UV irradiation, affect to different degrees the amount of UV-stimulated repair synthesis, and inhibit recovery of UV-irradiated nonreplicative λ phage (14Crumplin G.C. Carcinogenesis. 1981; 2: 157-160Crossref PubMed Scopus (32) Google Scholar, 15Sternglanz R. DiNardo S. Voelkel K.A. Nishimura Y. Hirota Y. Becherer K. Zumstein L. Wang J.C. Proc. Natl. Acad. Sci. U. S. A. 1981; 78: 2747-2751Crossref PubMed Scopus (194) Google Scholar, 16Purdy M.A. Yeilding L. Antimicrob. Agents Chemother. 1976; 10: 182-184Crossref PubMed Scopus (2) Google Scholar, 17Simon T. Masker W.E. Hanawalt P.C. Biochim. Biophys. Acta. 1974; 349: 271-274Crossref PubMed Scopus (21) Google Scholar, 18Hays J.B. Boehmer S. Proc. Natl. Acad. Sci. U. S. A. 1978; 80: 4125-4129Crossref Scopus (38) Google Scholar). These observations give a hint of the existence of the topological aspect of NER in vivo. However, the effect of damaged DNA topological state on and involvement of topoisomerases in NER in E. coli have received so far very limited biochemical characterization (19Friedberg E.C. Walker G.C. Siede W. DNA Repair and Mutagenesis. ASM Press, Washington, D. C.1995: 218Google Scholar, 20Munn M. Rupp D. J. Biol. Chem. 1991; 266: 24748-24756Abstract Full Text PDF PubMed Google Scholar, 21Backendorf C. Olsthoorn R. van de Putte P. Nucleic Acids. Res. 1989; 17: 10337-10351Crossref PubMed Scopus (11) Google Scholar, 22Pedrini A.M. Ciarocchi G. Proc. Natl. Acad. Sci. U. S. A. 1983; 80: 1787-1791Crossref PubMed Scopus (26) Google Scholar). In this report, we addressed this question using the in vitro system including Uvr proteins and topoisomerases. This topodynamic (23Kozyavkin S. Slesarev A.I. Malkhosyan S.R. Panyutin I.G. Eur. J. Biochem. 1990; 191: 105-113Crossref PubMed Scopus (10) Google Scholar, 24Kovalsky O.I. Kozyavkin S.A. Slesarev A.I. Nucleic Acids Res. 1990; 18: 2801-2805Crossref PubMed Scopus (32) Google Scholar) system allows for the differential regulation of the uvDNA topological state. It was found that highly positively supercoiled uvDNA generated by UvrA2B1 helix-tracking activity in the presence of only E. coli topo I is not incised by Uvr(A)BC, whereas it is efficiently incised by Micrococcus luteus UV endo. The addition to this reaction mixture of enzymatic activities removing positive supercoils (E. coli gyrase or eukaryotic topo I) results in restoration of the incision of uvDNA by Uvr(A)BC. The inability of Uvr(A)BC to incise highly positively supercoiled uvDNA is due to the inhibition of UvrAB-dependent incision intermediates associated with the DNA substrate conformational change (25Oh E.Y. Grossman L. Nucleic Acids Res. 1986; 14: 8557-8571Crossref PubMed Scopus (46) Google Scholar). The results are discussed in terms of the influence of DNA topology on the process of Uvr(A)BC damage recognition and incision as well as in terms of the applicability of this in vitro topodynamic system for study of the topological aspect of NER and its interaction with other DNA topology-involved cellular processes." @default.
• W2085703356 created "2016-06-24" @default.
• W2085703356 creator A5026416444 @default.
• W2085703356 creator A5031410215 @default.
• W2085703356 creator A5085808823 @default.
• W2085703356 date "1996-12-01" @default.
• W2085703356 modified "2023-10-14" @default.
• W2085703356 title "The Topodynamics of Incision of UV-irradiated Covalently Closed DNA by the Escherichia coli Uvr(A)BC Endonuclease" @default.
• W2085703356 cites W1481855462 @default.
• W2085703356 cites W1522275893 @default.
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