Search PubMed⌕ Search

Biomedical subjects

N Otsuji

Publications and source records attributed to N Otsuji.

33 records · Page 2Linked to original sources
PubMed1975

Ultraviolet light sensitivity of Escherichia coli K-12 strains carrying ruv mutations in combination with uvrA or lon mutant alleles.

Strains of Escherichia coli K12 have been prepared that carry the ruv mutation in combination with lon or uvrA mutant alleles. The ruv minus uvrA minus double mutant is more sensitive to ultraviolet light than the urvA minus single mutant, whereas the strain with ruv and ion mutations shows the same sensitivity to ultraviolet light as the ruv minus single mutant.

Alleles↗
PubMed1975

Location of the Escherichia coli K-12 ruv gene affecting septum formation after inhibition of deoxyribonucleic acid synthesis.

Escherichia coli ruv gene was located at 36.1 min on the chromosome by P1 transduction experiments and the gene order his - supD - uvrC, dar4 - ruv - eda - fadD - pps was proposed. Complementation analysis by an F' factor carrying genes in the his region indicated that ultraviolet light sensitivity genes, ruv and uvrC, consist of different cistrons and wild-type alleles of these genes are dominant over the mutant alleles.

Alleles↗
PubMed1974

Isolation and characterization of an Escherichia coli ruv mutant which forms nonseptate filaments after low doses of ultraviolet light irradiation.

Two ultraviolet light (UV)-sensitive mutants have been isolated from Escherichia coli K-12. These mutants, designated RuvA(-) and RuvB(-), were controlled by a gene located close to the his gene on the chromosome map. They were sensitive to UV (10- to 20-fold increase) and slightly sensitive to gamma rays (3-fold increase). Host cell reactivation, UV reactivation and genetic recombination were normal in these mutants. Irradiation of the mutants with UV resulted in the production of single-strand breaks in deoxyribonucleic acid, which was repaired upon incubation in a growth medium. After UV irradiation, these mutants resumed deoxyribonucleic acid synthesis at a normal rate, as did the parent wild-type bacteria, and formed nonseptate, multinucleate filaments. From these results we concluded that the mutants have some defect in cell division after low doses of UV irradiation, similar to the lon(-) or fil(+) mutant of E. coli. The ruv locus was divided further into ruvA and ruvB with respect to nalidixic acid sensitivity and the effect of minimal agar or pantoyl lactone on survival of the UV-irradiated cell. The ruvB(-)mutant was more sensitive to nalidixic acid than were ruvA(-) and the parent strain. There was a great increase in the surviving fraction of the UV-irradiated ruvB(-) mutant when it was plated on minimal agar or L agar containing pantoyl lactone. No such increase in survival was observed in the ruvA(-) mutant.

Agar↗
PubMed1972

Deoxyribonucleic acid damage by monofunctional mitomycins and its repair in Escherichia coli.

Exposure of Escherichia coli to the antibiotic mitomycin C (MTC) at a concentration of 0.5 mug/ml caused cross-linkage between complementary strands of deoxyribonucleic acid (DNA). Derivatives of mitomycin, 7-methoxymitosene (7-MMT) and decarbamoyl mitomycin C (DCMTC), at a level as high as 20 mug/ml formed no cross-links between DNA strands. Ultraviolet light-sensitive mutants of E. coli K-12 bearing uvrA, uvrB, uvrC, or recA mutations were more sensitive to the lethal action of 7-MMT and of DCMTC than was the wild-type strain. Treatment of wild-type cells with these antibiotics resulted in the production of single-strand breaks in DNA, which were repaired upon incubation in a growth medium. Such breaks in DNA were not produced in the uvrA and the uvrB mutants. In the uvrC mutant, single-strand breaks were produced by 7-MMT or by DCMTC, but these breaks were not repaired upon incubation. These results are discussed in connection with the mechanism for removal of pyrimidine dimers in ultraviolet-irradiated bacteria.

Carbon Isotopes↗
PubMed1972

[Drug resistance].

Explore the source record for details and available documents.

Anti-Bacterial Agents↗
PubMed1968

Properties of mitomycin C-sensitive mutants of Escherichia coli K-12.

Strains hypersensitive to mitomycin C (MC) were isolated from Escherichia coli K-12 after treatment with nitrosoguanidine. Of 43 MC-sensitive strains tested for their ultraviolet light (UV) sensitivity and for their ability to reactivate UV-inactivated lambda phage, 38 were found to be insensitive to UV irradiation and to be able to reactivate UV-irradiated bacteriophage lambda. Some properties of the MC-sensitive, uvr(+) mutants were analyzed. Synthesis of deoxyribonucleic acid (DNA) in MC-sensitive, uvr(+) mutants was inhibited at a lower concentration of MC than in the wild-type strain. Mutant cells, labeled with (3)H-thymidine and then exposed to MC, released radioactivity as low molecular weight compounds. The amount of radioactivity released was the same as that from the wild-type strain. MC-sensitive, uvr(+) mutants, as well as the corresponding wild-type strain, were equally susceptible to induction of prophage phi80 by UV irradiation. However, MC induction of prophage was achieved in MC-sensitive, uvr(+) mutants at a lower concentration of the antibiotic than in the wild-type strain. Genetic experiments indicated that a gene controlling MC sensitivity is located close to that determining lactose fermentation of E. coli. It is situated on episome F'13, and the wild type is dominant to the MC-sensitive allele.

Coliphages↗
PubMed1968

Effect of mutation to streptomycin resistance on amber suppressor genes.

Three classes of nonidentical streptomycin-resistant mutations were distinguished in Escherichia coli by their effect on the efficiency of suppression by an amber suppressor gene, sup E. The first class of mutation caused a strong restriction in efficiency of suppression of an amber codon in various cistrons of phage lambda and in an alkaline phosphatase structural gene of E. coli. The second class caused weak restriction, and the third class caused no restriction. The restrictive effect of the streptomycin resistance mutation of the first class on the sup E gene was reduced by addition of streptomycin. This mutation had little effect on efficiencies of suppression by amber suppressor genes sup D and sup F. Analyses on the alkaline phosphatase formed in the suppressor strain indicated that mutation to restrictive streptomycin resistance causes a reduction in translation of the amber codon in the alkaline phosphatase structural gene.

Alkaline Phosphatase↗