Enhanced generation of A:T→T:A transversions in a recA730 lexA51(Def) mutant of Escherichia coli

Watanabe-Akanuma, Mie; Woodgate, Roger; Ohta, Toshihiro

doi:10.1016/s0027-5107(96)00189-3

Cited by 33 publications

(34 citation statements)

References 24 publications

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“…Chlorate resistance is caused by any mutation that inactivates genes involved in the synthesis or uptake of molybdate or nitrate reductase (base pair substitutions, frameshifts, insertions, deletions, etc.). The polymerases Pol II, Pol IV, and Pol V generate frameshift mutations and small deletions at a high rate (Rangarajan et al 1997;Watanabe-Akanuma et al 1997;Wagner and Nohmi 2000), suggesting that all three polymerases are proficient in creating mutations that will cause chlorate resistance (it is presently unknown what the mutational spectrum of SamAB is). In contrast to chlorate resistance mutations, nalidixic acid resistance and rifampicin resistance mutations are conferred by a limited number of specific base pair substitutions in the gyrA and rpoB genes, respectively.…”

Section: Discussionmentioning

confidence: 99%

Effect of Translesion DNA Polymerases, Endonucleases and RpoS on Mutation Rates inSalmonella typhimurium

Koskiniemi¹,

Hughes

Andersson³

2010

Genetics

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It has been suggested that bacteria have evolved mechanisms to increase their mutation rate in response to various stresses and that the translesion DNA polymerase Pol IV under control of the LexA regulon and the alternative sigma factor RpoS are involved in regulating this mutagenesis. Here we examined in Salmonella enterica serovar Typhimurium LT2 the rates for four different types of mutations (rifampicin, nalidixic acid, and chlorate resistance and Lac 1 reversion) during various growth conditions and with different levels of four translesion DNA polymerases (Pol II, Pol IV, Pol V, and SamAB) and RpoS. Constitutive derepression of the LexA regulon by a lexA(def ) mutation had no effect on Lac 1 reversion rates but increased the other three mutation rates up to 11-fold, and the contribution of the translesion DNA polymerases to this mutagenesis varied with the type of mutation examined. The increase in mutation rates in the lexA(def ) mutant required the presence of the LexA-controlled UvrB protein and endonucleases UvrC and Cho. With regard to the potential involvement of RpoS in mutagenesis, neither an increase in RpoS levels conferred by artificial overexpression from a plasmid nor long-term stationary phase incubation or slow growth caused an increase in any of the four mutation rates measured, alone or in combination with overexpression of the translesion DNA polymerases. In conclusion, mutation rates are remarkably robust and no combination of growth conditions, induction of translesion DNA polymerases by inactivation of LexA, or increased RpoS expression could confer an increase in mutation rates higher than the moderate increase caused by derepression of the LexA regulon alone.

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Section: Discussionmentioning

confidence: 99%

Effect of Translesion DNA Polymerases, Endonucleases and RpoS on Mutation Rates inSalmonella typhimurium

Koskiniemi¹,

Hughes

Andersson³

2010

Genetics

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“…In such strains, increased mutagenesis occurs in the absence of any DNA damaging treatment (untargeted mutagenesis). This mutagenesis, when occurring on the bacterial chromosome or FЈ episome, depends, like targeted mutagenesis, on the action of pol V, as the recA730-or recA441-induced mutator activities are not observed in umuDC mutants (16)(17)(18)(19). Interestingly, another type of untargeted mutagenesis does not depend on pol V and RecA, but instead on pol IV, the dinB gene product (9)(10)(11)(12).…”

mentioning

confidence: 99%

SOS mutator activity: Unequal mutagenesis on leading and lagging strands

Maliszewska-Tkaczyk

Jonczyk

Bialoskorska

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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A major pathway of mutagenesis in Escherichia coli is mediated by the inducible SOS response. Current models of SOS mutagenesis invoke the interaction of RecA and UmuD 2C proteins with a stalled DNA replication complex at sites of DNA lesions or poorly extendable terminal mismatches, resulting in an (error-prone) continuation of DNA synthesis. The precise mechanisms of SOS-mediated lesion bypass or mismatch extension are not known. Here, we have studied mutagenesis on the E. coli chromosome in recA730 strains. In recA730 strains, the SOS system is expressed constitutively, resulting in a spontaneous mutator effect (SOS mutator) because of reduced replication fidelity. We investigated whether during SOS mutator activity replication fidelity might be altered differentially in the leading and lagging strand of replication. Pairs of recA730 strains were constructed differing in the orientation of the lac operon relative to the origin of replication. The strains were also mismatch-repair defective (mutL) to facilitate scoring of replication errors. Within each pair, a given lac sequence is replicated by the leading-strand machinery in one orientation and by the laggingstrand machinery in the other orientation. Measurements of defined lac mutant frequencies in such pairs revealed large differences between the two orientations. Furthermore, in all cases, the frequency bias was the opposite of that seen in normal cells. We suggest that, for the lacZ target used in this study, SOS mutator activity operates with very different efficiency in the two strands. Specifically, the lagging strand of replication appears most susceptible to the SOS mutator effect.

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“…Copyright: As is known, untargeted mutagenesis is characterized by a high percentage of education transversions [34,36,66].…”

Section: /14mentioning

confidence: 99%

“…The mutations that result from incorrect bases are often targeted; that is, they occur at the same position as the photoproduct [26,27]. Sometimes mutations are formed in the vicinity of damage, a process that is termed untargeted mutagenesis [19,20,[28][29][30][31][32][33].Untargeted mutations currently called mutations appearing on so-called "undamaged" DNA sites [19,20,[28][29][30][31][32][33][34][35][36]. Untargeted mutagenesis requires the same proteins that are required for translesion synthesis [34].…”

Section: Introductionmentioning

confidence: 99%

“…Untargeted mutagenesis occurs at SOS replication and error-prone DNA synthesis [19]. Untargeted mutagenesis is characterized by a high rate of education of transversions [19,34,36]. It is assumed that untargeted base substitution mutations formed on undamaged DNA sites in result in random errors of DNA polymerases [19,20,[28][29][30][31][32][37][38][39].…”

Section: Introductionmentioning

confidence: 99%

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A Polymerase Tautomeric Model for Radiation Induced Bystander Effects: A Model for Untargeted Base Substitution Mutagenesis during Error Prone and SOS Replication of Double Stranded DNA Containing Thymine and Adenine in Rare Tautomeric Forms

Grebneva¹

2017

IJMBOA

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Currently, untargeted mutations are studied in the context of bystander effects. Up to now the nature and mechanisms of formation of untargeted mutations is poorly understood. Untargeted base substitution mutations are base substitution mutations then one or some nucleotides are inserted in DNA molecule on, so called, undamaged sites of DNA. Here the polymerase-tautomeric models of ultraviolet mutagenesis and bystander effects are developed. The mechanisms of untargeted base substitution mutations formation caused by cis-syn cyclobutane thymine dimers and bases pairs of adenine-thymine or thymine-adenine in rare tautomeric forms that are in small neighbor from any cyclobutane dimers are proposed. Five rare tautomeric forms may form for thymine and adenine. These rare tautomeric forms will be stable if corresponding nucleotides are part of cyclobutane pyrimidine dimers or are in small neighbor of the cyclobutane dimers and during DNA synthesis. Structural analysis of bases incorporation shown that adenine in rare tautomeric form A 1

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Enhanced generation of A:T→T:A transversions in a recA730 lexA51(Def) mutant of Escherichia coli

Cited by 33 publications

References 24 publications

Effect of Translesion DNA Polymerases, Endonucleases and RpoS on Mutation Rates inSalmonella typhimurium

Effect of Translesion DNA Polymerases, Endonucleases and RpoS on Mutation Rates inSalmonella typhimurium

SOS mutator activity: Unequal mutagenesis on leading and lagging strands

A Polymerase Tautomeric Model for Radiation Induced Bystander Effects: A Model for Untargeted Base Substitution Mutagenesis during Error Prone and SOS Replication of Double Stranded DNA Containing Thymine and Adenine in Rare Tautomeric Forms

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