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A Sono

Publications and source records attributed to A Sono.

14 recordsLinked to original sources
PubMed1994

A meiotic DNA polymerase from a mushroom, Agaricus bisporus.

A meiotic DNA polymerase [DNA nucleotidyltransferase (DNA-directed), EC 2.7.7.7], which likely has a role in meiotic DNA repair, was isolated from a mushroom, Agaricus bisporus. The purified fraction displays three bands in SDS/PAGE, at molecular masses of 72 kDa, 65 kDa and 36 kDa. Optimal activity is at pH 7.0-8.0 in the presence of 5 mM Mg2+ and 50 mM KCl and at 28-30 degrees C, which is the temperature for meiosis. This enzyme is resistant to N-ethylmaleimide and sensitive to 2',3'-dideoxythymidine 5'-triphosphate, suggesting that it is a beta-like DNA polymerase. These characteristics are similar to those of Coprinus DNA polymerase beta [Sakaguchi and Lu (1982) Mol. Cell. Biol. 2, 752-757]. In Western-blot analysis, the antiserum against the Coprinus polymerase reacts only with the 65 kDa band, which coincides with the molecular mass of the Coprinus polymerase. Western-blot analysis also showed that the antiserum could react with crude extracts not only from the Agaricales family, to which Agaricus and Coprinus belong, but also from different mushroom families and Saccharomyces. The Agaricus polymerase activity can be found only in the meiotic-cell-rich fraction, but the enzyme is also present in the somatic cells in an inactive state.

Agaricus↗
PubMed1993

A meiotic DNA polymerase from Coprinus cinereus: further purification and characterization.

A meiotic DNA polymerase that is present at a high level of activity in meiotic cells of a basidiomycete, Coprinus cinereus, was purified to near homogeneity using synthetic RNA homopolymer [poly(C)] cellulose column chromatography. This report presents the first extensive purification and characterization of any eukaryotic DNA polymerase having a role in meiosis. This enzyme is a single polypeptide with a molecular mass of 65,000. Activity in this enzyme requires magnesium ions and occurs at an optimal pH of 7.5. It is strongly inhibited by dideoxythymidine triphosphate but is relatively insensitive to aphidicolin and N-ethylmaleimide and can use poly(C)/oligo(dG)12-18 as a template-primer. Polymerase activity can be found only in cells at meiotic prophase, even though the enzyme has been identified in somatic cells in an inactive state using immunoblot analysis. Its distinctive distribution makes possible a genetic and biochemical analysis of functional role of a meiotic DNA polymerase in meiotic recombination, repair and synthesis.

Aphidicolin↗
PubMed1989

[Mutagenicity studies of miporamicin].

Mutagenic activity of miporamicin (MPM), a new macrolide antibiotic for animal use, was examined using the reversion test with bacteria, the chromosomal aberration test with mammalian cells in culture and the micronucleus test with rodents. In the reversion test, MPM exhibited severe growth inhibition effect on the test bacteria but caused no increase of revertant colonies over the baseline levels, alone or in combination with S 9 mixture. In the chromosome aberration test, MPM induced a medium grade increase of chromosome aberrations at high concentrations, but induced no increase of polyploid cells over the control level. In the micronucleus test, MPM had no effect on induction of micronucleated polychromatic erythrocyte even at the 1/2 LD50 dose. From these results, we concluded that MPM has no effect on the induction of point mutations but has a weak clastogenicity which is detectable only by in vitro tests.

Animals↗
PubMed1988

Isolation and characterization of Chinese hamster cell line resistant to monofunctional alkylating agents.

A clonal derivative of a Chinese hamster Don D-6 cell line resistant to methyl methane sulfonate (MMS) has been isolated following mutagenesis by ethyl methane sulfonate (EMS). The clone, designated as MMSr-1, exhibited high resistance to killing by the monofunctional alkylating agents MMS and EMS. This characteristic had not been acquired by a transient adaptation to the alkylating agents but was found to be a stable heritable trait. MMSr-1 was more sensitive to high-molecular-weight chemicals, such as colchicine and puromycin, than Don D-6. Both MMSr-1 and its parental cells showed the same ability to take up radioactive MMS. The resistance of MMSr-1 appears not to be due to altered uptake of MMS. The resistance was accompanied by low chromosomal aberration and sister chromatid exchange (SCE) induction but not by mutability. Protein synthesis inhibitors such as cycloheximide and puromycin reduced the resistance to the same level as that in Don D-6. SCE induction by MMS in this clone was not antagonized by the protein synthesis inhibitors, whereas mutagenesis was reversed to the normal parental cell level by these inhibitors. Aphidicolin, a DNA-synthesis inhibitor, exhibited no such effects. These results suggest that MMSr-1 might have modified repair capacity, which can be normalized by treatment with the protein-synthesis inhibitors, for lethal DNA damage by monofunctional alkylating agents, and that SCE formation by the alkylating agents is closely correlated with chromosomal aberration and cell lethality.

Alkylating Agents↗
PubMed1988

Inhibition of protein synthesis does not antagonize induction of UV-induced sister-chromatid exchange in xeroderma pigmentosum cells.

Cycloheximide strongly antagonizes the induction of sister-chromatid exchanges by ethyl methanesulfonate or mitomycin C in human skin fibroblast and xeroderma pigmentosum cells (group A). Analogous behavior has been observed in several other species including Chinese hamster and plant cells. This report documents an exception to that pattern: cycloheximide fails to antagonize UV-induced sister chromatid exchange in xeroderma pigmentosum cells, whereas it does in normal human skin fibroblast cells. A genetic defect in these cells is postulated to alter the UV-mediated DNA recombination process.

Cells, Cultured↗
PubMed1986

The influence of a protein synthesis inhibitor on sister-chromatid exchange in the plant Vicia faba.

Cycloheximide strongly antagonizes the induction of sister-chromatid exchange by mitomycin C in Vicia faba root tips. This behavior is analogous to that previously observed in mammalian cells (Sono and Sakaguchi, 1981) and suggests that newly synthesized protein is also required for recombination between sister DNA molecules in plants. Conversely hydroxyurea is shown to increase the frequency of both spontaneous and induced sister-chromatid exchange. Based on these results, possible mechanisms underlying sister-chromatid exchange formation in plants are discussed with special emphasis on the absence of DNA polymerase beta in somatic tissues.

Chromosome Aberrations↗
PubMed1986

[Mutation frequency test for isepamicin (HAPA-B)].

Mutation frequency tests for isepamicin (HAPA-B), a new aminoglycoside antibiotic, were carried out using Salmonella typhimurium strains TA98, TA100, TA1535 and Escherichia coli WP2uvrA. After a 30-minute exposure of bacterial cells at 37 degrees C to HAPA-B in a buffer solution, the cells were washed twice with a buffer solution to minimize the cytotoxicity of the drug. Then washed cells were inoculated on minimum glucose agar plates to determine mutation frequency. The results should no significant increase in mutation frequency with increasing HAPA-B concentration; suggesting that the drug has no mutagenicity detectable by this test system.

Escherichia coli↗
PubMed1986

[Mutagenicity tests for isepamicin (HAPA-B)].

To detect mutagenic activity of isepamicin (HAPA-B), a new aminoglycoside antibiotic, we carried out several mutagenicity tests using microorganisms and cultured mammalian cells. Effects of the antibiotic on DNA-lesion induction and repair were examined using the Rec-assay with Bacillus subtilis and a sister-chromatid exchange test with cultured Chinese hamster cells. The drug caused no increase of mutagenicity indices in both tests, suggesting that the antibiotic has no DNA-damaging effect. To further investigate the effect of HAPA-B on gene-mutation, we performed the Ames Salmonella/microsome plate assay and the thioguanine resistance mutation test using cultured Chinese hamster cells. In both tests, the antibiotic induced no increase of mutation frequencies over spontaneous levels. Clastogenic activities of HAPA-B and its effect on chromosome disjunction were examined by the chromosomal aberration test using cultured Chinese hamster cells. After a short- or long-time exposure, the antibiotic induced neither structural chromosome aberrations nor an increase in the number of tetraploid cells. The negative results from these five test systems with different mechanisms strongly suggest the safety of HAPA-B regarding mutagenicity.

Animals↗
PubMed1984

Isolation of Chinese hamster cells hyposensitive to ethyl methanesulfonate and their characterization in induction and antagonization of sister-chromatid exchanges.

To better understand the molecular events involved in the formation of SCEs and mutations, 3 clonal sublines were established from a Chinese hamster cell line, Don D-6, on the basis of hyposensitivity to killing by ethyl methanesulfonate. These sublines, referred to as T80-4, T80-6 and T80-7, exhibited greatly altered karyotypes and altered frequencies of SCEs and mutations. These sublines were also less sensitive to chemical mutagens and ultraviolet irradiation as indicated by reduced frequencies of SCEs. This lower sensitivity was not due to differences in the rate of cell proliferation or to a cellular adaptive response. The rate of chemically- or UV-induced SCEs in these sublines did not always relate to cellular ploidy levels. The recent observation that, under constant experimental conditions, the rate of SCEs is a function of cellular ploidy level was not observed for these sublines. Thus, there appeared to be a modification in the intrinsic process of SCE formation. We reported previously that protein synthesis is essential for the induction of mutation as well as for SCE in Don D-6. However, the ability of cycloheximide (CH) to antagonize EMS-induced SCEs and mutations in the T80-7 subline was much lower than in the parental cells or in other sublines. The cells of this subline might contain a defective protein or a modification of the process for which the protein is required.

Animals↗
PubMed1982

Antagonization by cycloheximide of ethyl methanesulfonate-induced 6-thioguanine-resistant mutation and sister-chromatid exchanges.

We studied the effect of cycloheximide (CH) on the induction of mutation and sister-chromatid exchanges (SCEs) in ethyl methanesulfonate (EMS)-treated Chinese hamster cells. At 10(-6)M, CH strongly antagonized the induction of mutation and SCEs and cell survival increased. This suggests that protein synthesis is essential for the induction of mutation as well as SCEs. Results of experiments in which CH treatment preceded or followed exposure to mutagens were similar with respect to the response curves obtained for mutation and SCEs.

Animals↗
PubMed1982

Effects of colchicine, Colcemid and vincristine on ethyl methanesulfonate-induced sister chromatid exchanges and chromosomal aberrations in Chinese hamster cells.

The effect of colchicine, Colcemid and vincristine on ethyl methanesulfonate-induced sister chromatid exchanges and chromosomal aberrations was studied in Chinese hamster cells. The number of ethyl methanesulfonate-induced sister chromatid exchanges was markedly decreased with increasing doses of colchicine and vincristine. In the presence of colchicine, ethyl methanesulfonate-induced chromosomal aberrations increased; these were mainly breaks and fragmentations. The effects were most prominent at the earlier stage of the cell cycle. Colchicine, Colcemid and vincristine had no effect on spontaneous sister chromatid exchanges or chromosomal aberrations.

Animals↗
PubMed1981

Inhibition of protein synthesis antagonizes induction of sister-chromatid exchanges by exogenous agents.

Cycloheximide (CH) and puromycin (PM)strongly antagonize induction of sister-chromatid exchanges (SCEs) by exogenous agents regardless of the mechanism for initiating damage. 5-Bromodeoxyuridine (BUdR) substitution was used to monitor SCEs, but the background level of BUdR-induced SCEs was unaffected by the presence of protein inhibitors. Antagonism between DNA-damaging agents and protein inhibitors was strongest in euchromatic regions. Possible relationships between SCE formation and the mechanism of antagonism by protein inhibitors are discussed.

Animals↗
PubMed1981

[Mutagenicity tests on mequitazine (author's transl)].

Microbial backward mutation test, Ames Salmonella/microsome plate assay, on six bacterial strains (Salmonella typhimurium TA 98, 100, 1535, 1537, 1538 and E. coli WP 2uvrA) and micronucleus test in mice were carried out to detect mutagenic activity of mequitazine. Mequitazine caused no increases of revertants at doses from 1 to 1000 microgram/plate in every bacterial strains irrespective of metabolic activation. Similarly, mequitazine induced no significant increases of micronucleated polychromatic erythrocytes in mice over the control level at doses from 0.12 (clinical dose) to 48 mg/kg (approx. LD 50). From above results, we concluded that mequitazine has no mutagenic activity per se.

Animals↗