Characterization of Spontaneous Mutation in the ΔsoxR and SoxS Overproducing Strains of Escherichia coli

Yamamura, Eiji; Lee, Eun Hye; Kuzumaki, Akihiro; Uematsu, Norio; Nunoshiba, Tatsuo; Kawata, Masakado; Yamamoto, Kazuo

doi:10.1269/jrr.43.195

Cited by 4 publications

(1 citation statement)

References 32 publications

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“…3Ј exo), KK202 (mutS polA) and KK200 (mutS) strains Sites where incidences number more than three are listed. All the data are available from online supplemental Table S1 at http://www.biology.tohoku.ac.jp/»kazuo/07imai/ a Numbering is in accordance with Kitamura and Yamamoto (1996) in which 2993 is the Wrst A of the ATG start codon and 3727 is the last A of the TAA stop codon of the tonB gene b The KK1 column contains data from KK1 (mutS + polA + ) , TM31 (mutS + polA + ) (Kitamura et al 1995), EY5 (mutS + polA + oxyR) (Yamamura et al 2000), EY7 (mutS + polA + soxR) (Yamamura et al 2002), KM3 (mutS + polA + ruvAB) (Mashimo et al 2004), KM4 (mutS + polA + recG) (Mashimo et al 2004), KM5 (mutS + polA + ruvC) (Mashimo et al 2004), UA2 (mutS + polA + recJ) (Mashimo et al 2003) and UA3 (mutS + polA + recQ) (Mashimo et al 2003). The IMA101 (mutS polA1) column contains data from IMA101 and the derivatives with defective SOS polymerases (i.e., dinB, polB, and umuCD) .…”

Section: Resultsmentioning

confidence: 99%

Role of the 5´ → 3´ exonuclease and Klenow fragment of Escherichia coli DNA polymerase I in base mismatch repair

et al. 2007

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We have previously demonstrated that the Escherichia coli strain mutS DeltapolA had a higher rate of transition and minus frameshift mutations than mutS or DeltapolA strains. We argued that DNA polymerase I (PolI) corrects transition mismatches. PolI, encoded by the polA gene, possesses Klenow and 5' --> 3' exonuclease domains. In the present study, rates of mutation were found to be higher in Klenow-defective mutS strains and 5' --> 3' exonuclease-defective mutS strains than mutS or polA strains. The Klenow-defective or 5' --> 3' exonuclease-defective mutS strains showed a marked increase in transition mutations. Sites of transition mutations in mutS, Klenow-defective mutS and 5' --> 3' exonuclease-defective mutS strains are different. Thus, it is suggested that, in addition to mutS function, both the Klenow and 5' --> 3' exonuclease domains are involved in the decrease of transition mutations. Transition hot and warm spots in mutS+ polA+ strains were found to differ from those in mutS and mutS DeltapolA strains. We thus argue that all the spontaneous transition mutations in the wild-type strain do not arise from transition mismatches left unrepaired by the MutS system or MutS PolI system.

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Section: Resultsmentioning

confidence: 99%

Role of the 5´ → 3´ exonuclease and Klenow fragment of Escherichia coli DNA polymerase I in base mismatch repair

et al. 2007

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Frameshift Mutations Produced by 9-Aminoacridine in Wild-Type, uvrA and recA Strains of Escherichia coli; Specificity Within a Hotspot

Acharya

Abu-Nasr²,

Kawaguchi

et al. 2007

JRR

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The endogenous tonB gene of Escherichia coli was used as a target for 9-aminoacridine-induced mutations that were identified in recA(-) and uvrA(-) cells. The cytotoxicity of 9-aminoacridine was enhanced in the uvrA and recA strains compared to the wild-type strain, and the mutagenicity of 9-aminoacridine in the uvrA and recA strains was similar to that in the wild type. For all three strains, the most common mutations were minus frameshifts in repetitive G:C base-pairs followed by minus frameshifts in nonrepetitive G:C base-pairs. 9-aminoacridine-induced minus frameshifts in the wild-type strain were distributed with several hot and warm spots. These sites were also hot and warm spots for minus frameshifts in the recA and uvrA stains. Furthermore, they were hot and warm sites in a 9-aminoacridine-treated strain carrying the target tonB gene oriented in the opposite direction. 9-Aminoacridine is known to interact with DNA to form intercalations which are involved in minus frameshift mutagenesis. In this study, we therefore argue that 1) 9-aminoacridine can induce bulky DNA lesions which are excised by nucleotide excision repair and not involved in mutagenesis, 2) the presence or absence of a recA-dependent repair pathway does not influence the mutagenic effect of 9-aminoacridine, and 3) both leading strand and lagging strand replication equally produce minus frameshifts, therefore gene orientation is not an important determinant of the formation of hot and warm spots by 9-aminoacridine.

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CPD Photolyase Gene from Spinacia oleracea : Repair of UV-Damaged DNA and Expression in Plant Organs

Yoshihara

Imaki

Hori

et al. 2005

JRR

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The UV-B radiation contained in solar radiation has deleterious effects on plant growth, development and physiology. Specific damage to DNA caused by UV radiation involves the cyclobutyl pyrimidine dimers (CPD) and the pyrimidine (6-4) pyrimidone photoproducts. CPDs are repaired by CPD photolyase via a UV-A/blue light-dependent mechanism. The gene for the class II CPD photolyase has been cloned from higher plants such as Arabidopsis, cucumbers and rice. We isolated and characterized the cDNA and a genomic clone encoding the spinach class II CPD photolyase. The gene consisted of 3777 bases and 9 exons. The sequence of amino acids predicted from the nucleotide sequence of the cDNA of the gene was highly homologous to that of the higher plants listed above. When a photolyase-deficient Escherichia coli strain was transformed with the cDNA, photoreactivation activity was partially restored, by the illumination with photoreactivating light, resulting in an increased survival and decreased content of CPDs in the Escherichia coli genome. In both the male and female plants, the gene was highly expressed in leaves and flowers under the condition of 14-h light and 10-h dark cycle. The expression in the roots was quite low compared with the other organs.

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Characterization of Spontaneous Mutation in the ΔsoxR and SoxS Overproducing Strains of Escherichia coli

Cited by 4 publications

References 32 publications

Role of the 5´ → 3´ exonuclease and Klenow fragment of Escherichia coli DNA polymerase I in base mismatch repair

Role of the 5´ → 3´ exonuclease and Klenow fragment of Escherichia coli DNA polymerase I in base mismatch repair

Frameshift Mutations Produced by 9-Aminoacridine in Wild-Type, uvrA and recA Strains of Escherichia coli; Specificity Within a Hotspot

CPD Photolyase Gene from Spinacia oleracea : Repair of UV-Damaged DNA and Expression in Plant Organs

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