Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mutagen-induced intergenic and interallelic recombination as well as forward mutation were studied in one and the same strain of S. cerevisiae. In nontoxic dose ranges, the induction of mutants and recombinants was parallel after treatment with ethyl methanesulfonate (EMS), methyl methanesulfonate (MMS), N-methyl-N'-nitro-M-nitrosoguanidine (MNNG), triethylene melamine (TEM), 4-nitroquinoline 1-oxide (4-NQO), sodium nitrite (NaNO2), and 1-fluoro-2,4-dinitrobenzene (2,4-DNFB). Acridine orange (AO) after treatment without light induced recombinants, but reduced the frequency of spontaneous mutations. In combination with TEM, AO exerted the same effect, i.e., reduced its mutagenic effect and enhanced its recombinogenic effect. 4,5,6-Trichloro-2-(2,4-dichlorophenoxy) phenol (Cl5-predioxin) induced mutants and intergenic recombinants, but specifically reduced the spontaneous frequency of interallelic recombinants. In combination with TEM, it enhanced its mutagenic and intergenic recombinogenic effects but reduced its interallelic recombinogenic effect. The main conclusions of the present study, that is 1. Essentially similar lesions can lead to different genetic consequences, and 2. Induction of mutation and recombination are jointly correlated, i.e., suppression of mutations leads to an enhancement of recombinations, while suppression of recombinations leads to an enhancement of mutations, are used to set up a speculative concept for mutation and recombination induction in the diploid yeast cell during mitosis.
Mol Gen Genet 1979 Jan 10
PMID:Evidence that induction and suppression of mutations and recombinations by chemical mutagens in S. cerevisiae during mitosis are jointly correlated. 10 36

Embroys heterozygous for five recessive coat-color genes from the cross C 57 BL/6 J Han x T-stock were x-irradiated with 100/r o r treated in utero with 50 mg/3 kg methyl methanesulfonate (MMS) and ethyl methanesulfonate (EMS), respectively. Controls consisted of irradiated embryos of C 57 BL x C 57 BL matings homozygous wild-type for the genes under study, and non-treated offspring of both types of mating. The colors of the spots were observed in the adult fur were either due to expression of the recessive coat genes or were white. I. Irradiated and mutagen-treated offspring of C 57 BL x T-stock matings had almost exclusively nonwhite spots, distributed randomly over the mouse surface. 2. Irraidated offspring of C 57 BL x C 57 BL matings had only white spots which were always midventral. 3. In non-treated offspring of both types of mating no spot could be observed. After correcting for white midventral spots observed in the one type of control, the frequency of expression of one or the other of the recessive color genes is calculated to be about 11% for embryos irradiated with 100r or 101/2 days postconception, about 1% for embryos irradiated with 100r at 9 days postconception, about &% for embryos treated with 50 mg MMS/kg at 101/2 days postconception, and about 8% for embryos treated with 50 mg EMS/2 days postconception. It is discussed that the white midventral spots are preferentially the result of pigment cell killing, while the nonwhite spots are preferentially the result of gene mutations or recombinational processes like mitotic crossing over and mitotic gene conversion. Of numerical and structural chromosome aberrations only those come into question which are able to pass the filter of several mitoses. Therefore, the test system described is supposted to cover not only heitable DNA-alterations, but the whole spectrum of them.
Mol Gen Genet 1975 Jul 10
PMID:A mammalian spot test: induction of genetic alterations in pigment cells of mouse embryos with x-rays and chemical mutagens. 16 82

Twenty-eight X-linked, recessive mutations of Drosophila melanogaster conferring enhanced sensitivity to the monofunctional alkylating agent, methyl methanesulfonate, have been recoered and assigned to five complementation groups. These groups can be distinguished on the basis of map location and variations in the pattern of mutagen sensitivity. Allelism of members of one complementation group with the previously described meiotic mutant, mei-41, (Baker and Carpenter, 1972) as well as the frequent appearance of female infertility with mutagen sensitivity suggests associated defects in meiotic chromosome behavior or early embryogenesis. Examination of the mutagen sensitivity of double mutants has led to the formulation of a working model of DNA repair for this organism. Studies of a similar nature (Boyd et al., 1976) have identified five additional X chromosome complementation groups, suggesting that the genome of Drosophila melanogaster may contain many loci involved with mutagen sensitivity. The continued isolation and characterization of conditional mutants of this type promises future insights into the mechanisms of DNA replication, DNA repair and recombination in this complex higher eucaryote.
Mol Gen Genet 1976 Nov 24
PMID:Mutagen sensitivity of Drosophila melanogaster. III. X-linked loci governing sensitivity to methyl methanesulfonate. 18 78

It was found that yeast cells contain an endonuclease specific for apurinic sites in DNA which has no effect on DNA with normal strands or on strands with alkylated sites. The enzyme activity was studied in the RAD strain and in rad 6, rad 18-2 and rad 21 mutants, all very sensitive to MMS, as compared to the wild type. The level of endonuclease activity does not differ much between the tested strains, regardless of their differences in susceptibility to MMS. The enzyme activity is not induced by pretreatment of the cells with this mutagen.
Mol Gen Genet 1977 Jul 20
PMID:Endonuclease for apurinic sites in yeast. Comparison of the enzyme activity in the wild type and in rad mutants of Saccharomyces cerevisiae to MNS. 19 92

A mutant of Haemophilus influenzae which does not discriminate between low efficiency (LE) and high efficiency (HE) markers has been isolated. The mutant does not differ wild type in its sensitivity to ultraviolet radiation, methyl methanesulfonate (MMS) mitomycin C, and nitrous acid. Spontaneous mutation frequencies for three loci studied are 10- to 30-fold higher in the mutant than in the wild type strain. Low- and high-efficiency transforming markers are equally UV-resistant when assayed on this mutant. This mutant is thus similar to the hex mutant of Streptococcus pneumoniae.
Mol Gen Genet 1979 Sep
PMID:A hex mutant of Haemophilus influenzae. 31 97

The drug resistance plasmid pKM101 plays a mojor role in the Ames Salmonella/microsome carcinogen detecting system by enhancing chemical mutagenesis. It is shown that in Escherichia coli K-12 the plasmid pKM101 enhances both spontaneous and methyl methanesulfonate-caused reversion of an ochre mutation, bacterial survival after ultraviolet irradiation, and reactivation of ultraviolet-irradiated lambda in unirradiated cells. All these effects are shown to be dependent on the recA+ lexA+ genotype but not on the recB+ recC+ or recF+ genotypes. The recA lexA-dependence of the plasmid-mediated repair and mutagenesis suggests an interaction with the cell's inducible error-prone repair system. The presence of pKM101 is shown to cause an additional increase in methyl methanesulfonate mutagenesis in a tif mutant beyond that caused by growth at 42 degrees. The presence of the plasmid raises the level of the Weigle-reactivation curve for the raactivation of ultraviolet-irradiated lambda in E. coli and causes a shif of the maximum to a higher UV fluence. These observations suggest that pKM101 does not exert its effects by altering the regulation of the cell's error-prone repair system but rather by supplying a mechanistic component or components.
Mol Gen Genet 1977 Mar 28
PMID:Plasmid (pKM101)-mediated enhancement of repair and mutagenesis: dependence on chromosomal genes in Escherichia coli K-12. 32 91

Selection for defective reversion induction, after UV treatment of E. coli K 12, yielded uvm mutants. These mutants exhibited highly reduced or no UV mutability for all loci tested although they were moderately and normally mutable by X-rays and EMS, respectively. Uvm mutations confer only a slight sensitivity to killing by UV and X-rays and no clear sensitivity to the lethal effect of HN2, EMS or MMS. Growth and viability of untreated uvm cells were normal. The properties of uvm mutants are discussed in relation to those of other relevant mutant types and to some actual problems of induced mutagenesis.
Mol Gen Genet 1978 Sep 20
PMID:Uvm mutants of Escherichia coli K12 deficient in UV mutagenesis. I. Isolation of uvm mutants and their phenotypical characterization in DNA repair and mutagenesis. 36 69

The formation and repair of double-strand breaks induced in DNA by MMS was studied in haploid wild type and MMS-sensitive rad6 mutant strains of Saccharomyces cerevisiae with the use of the neutral and alkaline sucrose sedimentation technique. A similar decrease in average molecular weight of double-stranded DNA from 5--6 X 10(8) to 1--0.7 X 10(8) daltons was observed following treatment with 0.5% MMS in wild type and mutant strains. Incubation of cells after MMS treatment in a fresh drug-free growing medium resulted in repair of double-strand breaks in the wild type stain, but only in the exponential phase of growth. No repair of double-strand breaks was found when cells of the wild type strain were synchronized in G-1 phase by treatment with alpha factor, although DNA single-strand breaks were still efficiently repaired. Mutant rad6 which has a very low ability to repair MMS-induced single-strand breaks, did not repair double-strand breaks regardless of the phase of growth. These results suggest that (1) repair of double-strand breaks requires the ability for single-strand breaks repair, (2) rejoining of double-strand breaks requires the availability of two homologous DNA molecules, this strongly supports the recombinational model of DNA repair.
Mol Gen Genet 1979 Jan 02
PMID:Repair of MMS-induced DNA double-strand breaks in haploid cells of Saccharomyces cerevisiae, which requires the presence of a duplicate genome. 36 92

The presence of the drug resistance plasmid pKM101 restored the ability of Escherichia coli umuC mutant strains to be mutated by methyl methanesulfonate. Inducible (Weigle) reactivation of ultraviolet-irradiated bacteriophage lambda was not observed in uvrA6 umuC mutant strains lacking pKM101 but was observed if the plasmid was present in the strains. In a uvrA+ umuC36 strain pKM101 increased the efficiency of the Weigle reactivation process. Plasmid-mediated UV-resistance and plasmid-mediated phage reactivation were observed in umuC(pKM101) strains both in uvrA+ and uvrA6 backgrounds. No restoration of methyl methanesulfonate mutability by pKM101 was observed in umuC36 recA56 strains. pKM101 mutants unable to enhance mutagenesis in umuC+ backgrounds also had no effect on methyl methanesulfonate mutagenesis in umuC mutant strains. Neither a umuC mutation nor the presence of pKM101 affected the UV induction of protein X, the recA protein. Hypotheses relating the mode of action of pKM101 to the process of mutagenesis and inducible phage reactivation are discussed.
Mol Gen Genet 1979 Apr 17
PMID:Mutagenesis and repair deficiencies of Escherichia coli umuC mutants are suppressed by the plasmid pKM101. 37 21

The ability to remove ultraviolet (UV)-induced pyrimidine dimers from the nuclear DNA of yeast was examined in two radiation-sensitive (rad) mutants and one methyl methanesulfonate-sensitive (mms) mutant of the yeast Saccharomyces cerevisiae. The susceptibility of DNA from irradiated cells to nicking by an endonuclease activity prepared from crude extracts of Micrococcus luteus was used to measure the presence of dimers in DNA. The rad7, rad14 and mms19 mutants were found to be defective in their ability to remove UV-induced dimers from nuclear DNA. All three mutants belong to the same epistatic group as the other mutants involved in excision-repair. All three mutants show enhanced UV-induced mutations. The rad14 mutant also shows epistatic interactions with genes in the other two UV repair pathways.
Mol Gen Genet 1979 Nov
PMID:Three additional genes involved in pyrimidine dimer removal in Saccharomyces cerevisiae: RAD7, RAD14 and MMS19. 39 38


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