Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents
Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggest...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Attfield, P.V. [verfasserIn] Pinney, R.J. [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1985 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2006 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: FEMS microbiology letters - Federation of European Microbiological Societies ; GKD-ID: 114439X, Oxford [u.a.] : Wiley-Blackwell, 1977, 28(1985), 3, Seite 0 |
| Übergeordnetes Werk: |
volume:28 ; year:1985 ; number:3 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1111/j.1574-6968.1985.tb00807.x |
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NLEJ239766385 |
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| 245 | 1 | 0 | |a Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents |
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| 520 | |a Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. | ||
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10.1111/j.1574-6968.1985.tb00807.x doi (DE-627)NLEJ239766385 DE-627 ger DE-627 rakwb Attfield, P.V. verfasserin aut Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents Oxford, UK Blackwell Publishing Ltd 1985 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| R plasmid stability Pinney, R.J. verfasserin aut In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS microbiology letters Oxford [u.a.] : Wiley-Blackwell, 1977 28(1985), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927053 (DE-600)1501716-3 1574-6968 nnns volume:28 year:1985 number:3 pages:0 http://dx.doi.org/10.1111/j.1574-6968.1985.tb00807.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 28 1985 3 0 |
| spelling |
10.1111/j.1574-6968.1985.tb00807.x doi (DE-627)NLEJ239766385 DE-627 ger DE-627 rakwb Attfield, P.V. verfasserin aut Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents Oxford, UK Blackwell Publishing Ltd 1985 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| R plasmid stability Pinney, R.J. verfasserin aut In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS microbiology letters Oxford [u.a.] : Wiley-Blackwell, 1977 28(1985), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927053 (DE-600)1501716-3 1574-6968 nnns volume:28 year:1985 number:3 pages:0 http://dx.doi.org/10.1111/j.1574-6968.1985.tb00807.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 28 1985 3 0 |
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10.1111/j.1574-6968.1985.tb00807.x doi (DE-627)NLEJ239766385 DE-627 ger DE-627 rakwb Attfield, P.V. verfasserin aut Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents Oxford, UK Blackwell Publishing Ltd 1985 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| R plasmid stability Pinney, R.J. verfasserin aut In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS microbiology letters Oxford [u.a.] : Wiley-Blackwell, 1977 28(1985), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927053 (DE-600)1501716-3 1574-6968 nnns volume:28 year:1985 number:3 pages:0 http://dx.doi.org/10.1111/j.1574-6968.1985.tb00807.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 28 1985 3 0 |
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10.1111/j.1574-6968.1985.tb00807.x doi (DE-627)NLEJ239766385 DE-627 ger DE-627 rakwb Attfield, P.V. verfasserin aut Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents Oxford, UK Blackwell Publishing Ltd 1985 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| R plasmid stability Pinney, R.J. verfasserin aut In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS microbiology letters Oxford [u.a.] : Wiley-Blackwell, 1977 28(1985), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927053 (DE-600)1501716-3 1574-6968 nnns volume:28 year:1985 number:3 pages:0 http://dx.doi.org/10.1111/j.1574-6968.1985.tb00807.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 28 1985 3 0 |
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10.1111/j.1574-6968.1985.tb00807.x doi (DE-627)NLEJ239766385 DE-627 ger DE-627 rakwb Attfield, P.V. verfasserin aut Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents Oxford, UK Blackwell Publishing Ltd 1985 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| R plasmid stability Pinney, R.J. verfasserin aut In Federation of European Microbiological Societies ; GKD-ID: 114439X FEMS microbiology letters Oxford [u.a.] : Wiley-Blackwell, 1977 28(1985), 3, Seite 0 Online-Ressource (DE-627)NLEJ243927053 (DE-600)1501716-3 1574-6968 nnns volume:28 year:1985 number:3 pages:0 http://dx.doi.org/10.1111/j.1574-6968.1985.tb00807.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 28 1985 3 0 |
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Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents |
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Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. |
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Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. |
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Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ239766385</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506095839.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">120426s1985 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1111/j.1574-6968.1985.tb00807.x</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ239766385</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Attfield, P.V.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Involvement of Escherichia coli K-12 recombination functions in elimination of multicopy plasmid R6K by DNA-damaging agents</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">Oxford, UK</subfield><subfield code="b">Blackwell Publishing Ltd</subfield><subfield code="c">1985</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Drugs that damage DNA by different mechanisms eliminate an F-lac+ plasmid and multicopy plasmid R6K from Escherichia coli K-12 wild type (polA+rec+). However, low-copy plasmid R1 is refractory to elimination under identical conditions. R6K is not eliminated from a polA mutant, which suggests that curing is not due to reduced availability of DNA polymerase I for plasmid replication in cells undergoing DNA repair. R6K is eliminated almost three times faster from a recBrecC sbcB mutant than from wild-type strains, whereas elimination from a recF mutant occurs at a rate similar to wild type. Hence, recombination may be involved in drug-mediated elimination of R6K, particularly in cells that carry out recF-dependent recombination exclusively.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="d">2006</subfield><subfield code="f">Blackwell Publishing Journal Backfiles 1879-2005</subfield><subfield code="7">|2006||||||||||</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">R plasmid stability</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pinney, R.J.</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">In</subfield><subfield code="a">Federation of European Microbiological Societies ; GKD-ID: 114439X</subfield><subfield code="t">FEMS microbiology letters</subfield><subfield code="d">Oxford [u.a.] : Wiley-Blackwell, 1977</subfield><subfield code="g">28(1985), 3, Seite 0</subfield><subfield code="h">Online-Ressource</subfield><subfield code="w">(DE-627)NLEJ243927053</subfield><subfield code="w">(DE-600)1501716-3</subfield><subfield code="x">1574-6968</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:28</subfield><subfield code="g">year:1985</subfield><subfield code="g">number:3</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1111/j.1574-6968.1985.tb00807.x</subfield><subfield code="q">text/html</subfield><subfield code="x">Verlag</subfield><subfield code="z">Deutschlandweit zugänglich</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-DJB</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">28</subfield><subfield code="j">1985</subfield><subfield code="e">3</subfield><subfield code="h">0</subfield></datafield></record></collection>
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7.401101 |