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

A somatic cell genetic approach was used to study the role of cyclic nucleotides in adrenal steroidogenesis. 8-Bromoadenosine 3',5'-monophosphate (8BrcAMP) stimulated steroidogenesis (K'd=0.1 mM) in cultured mouse adrenocortical tumor cells (Clone Y1). In addition, 8BrcAMP inhibited Y1 cell growth and caused Y1 cell monolayers to assume a rounded morphology. As a consequence, 8BrcAMP (at concentrations greater than or equal to 0.4 mM) reduced the relative plating efficiency of Y1 cells to less than 10(-5). Y1 cells were mutagenized with ethyl methanesulfonate (300 microgram/ml) and grown in the presence of 0.4 mM 8BrcAMP. A surviving colony (8BrcAMPr-1) was shown to be resistant to growth inhibition (relative plating efficiency at 1.0 mM 8BrcAMP=50 percent)) and to morphological changes induced by 8BrcAMP. 8BrcAMPr-1 cells had diminished steroidogenic responses to cyclic nucleotides and to ACTH (less than or equal to 33 percent of maximum). In 8BrcAMP(R)-1 cells, adenylate cyclase activity remained responsive to ACTH, and cyclic AMP phosphodiesterase activity was not increased. These data suggest that 8BrcAMPr-1 cells are defective at a point common to cyclic AMP action on growth, morphology and steroidogenesis. The associated decrease in responsiveness of the steroidogenic pathway to ACTH suggests that ACTH-regulated steroidogenesis is via a cyclic nucleotide-mediated mechanism.
Mol Cell Endocrinol 1977 Aug
PMID:Isolation of mutant adrenocortical tumor cells resistant to cyclic nucleotides. 20 May 6

Treatment of bacteriophage T4 by ethyl methanesulfonate (EMS) caused more than a doubling in recombination between two rII markers. The functions of genes 47, 46, 32, 30, uvsX and y are known to be required for genetic recombination, and mutants defective in these genes were found to be more sensitive to inactivation by EMS than wild-type phage. This suggests that a recombinational pathway involving the products of these genes may be employed in repairing EMS induced lethal lesions. Genes 45 and denV are apparently not involved in recombination, and mutants defective in these genes were not EMS-sensitive. Gene 47, 46 and y mutants which were defective in the repair of EMS induced lethal lesions had no detectable deficiency in their ability to undergo EMS-induced mutation. This implies that recombinational repair of EMS lesions does not contribute substantially to EMS mutagenesis. The results obtained here with EMS are general similar to the results reported in the preceding paper with MNNG, suggesting that the lesions caused by both of these monofunctional alkylating agents may be eliminated by similar recombinational repair processes.
Mol Gen Genet 1978 Nov 29
PMID:Recombinational repair of alkylation lesions in phage T4. II. Ethyl methanesulfonate. 21 91

E. coli strains carrying the dam-3 and dam-4 mutations resulting in reduced levels of 6-methyladenine in the DNA have been found to be more sensitive to base analogue mutagenesis than dam+ strains. Mutagenesis by EMS was also found to be enhanced in dam- strains. Dam- mutants however were not found to be hypermutable by UV light. It is concluded that the dam- strains are deficient in the correct repair of mispairing lesions. The data are consistent with the hypothesis that 6-methyladenine residues in the DNA are involved in strand discrimination during mismatch correction.
Mol Gen Genet 1978 Jul 25
PMID:Induced mutagenesis in dam- mutants of Escherichia coli: a role for 6-methyladenine residues in mutation avoidance. 35 57

Invertase formation in the yeast Saccharomyces cerevisiae is subject to repression by hexoses in the growth medium. Mutagen-induced (ethyl methanesulfonate or N-methyl-N-nitro-nitrosoguanidine) invertase hyperproducer mutants have been derived from the SUC3 MAL3 strain EK-6B by selecting for their ability to grow on media containing the sugar raffinose plus 2-deoxy-D-glucose (2DG). Raffinose like sucrose is a betta-fructoside which can be hydrolyzed by yeast invertase (beta-fructoside which can be hydrolyzed by yeast invertase (beta-fructofuranoside fructohydrolase). These mutants, designated dgr, produce higher levels of invertase (pi-glucosidase levels are also elevated but to a lesser extent) under conditions normally repressing invertase biosynthesis in the parent. Invertases of mutants dgr2 and dgr3 are indistinguishable from that of EK-6B with respect to their Km's for sucrose and thermal labilities. Genetic studies revealed that dgr2 and dgr3 are recessive and unlinked to the SUC3 gene.
Mol Gen Genet 1978 Sep 08
PMID:Genetic control of invertase formation in Saccharomyces cerevisiae. II. Isolation and characterization of mutants conferring invertase hyperproduction in strain EK-6B carrying the SUC3 gene. 36 57

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

DNA of the streptococcal plasmid ERLI, determining resistance to erythromycin and lincomycin has been studied. The presence of satellite DNA component in streptococcal DNA has been demonstrated by dye-CsCl and CsCl density centrifugation, by chromatography of denatured-renatured DNA on the nitrocellulose and by electron microscopy. By all these methods the presence of covalently closed circular DNA molecules has been shown. Plasmid DNA has buoyant density in CsCl equal to 1.698 g/cm3 (GC content--38.8%), molecular weight (by electron microscopy) -- 19.8 Mdal; number of copies chromosomal genome equivalent is equal to about 4--4.5. Plasmid ERLI DNA was extracted from an original strain-carrier of plasmid ERLI, from a transduced strain which received plasmid ERLI as a result of transduction and lysogenization by phage "mo" and from the two antibiotic sensitive EMS mutants of resistant strain. Satellite DNA could not be isolated from a sensitive strain which served as a recipient in transduction experiments. The results obtained are in agreement with the literature on the molecular weight of the plasmid measured by the sedimentation analysis and with the previous genetic data on the antibiotic resistance within group A streptococci.
Mol Biol (Mosk)
PMID:[Isolation and characteristics of plasmids determining multiple antibiotic resistance in strains of group A streptococci]. 37 51

The molecular nature of lethal and semilethal mutations in the Pgd locus of D. melanogaster coding for 6-phosphogluconate dehydrogenase (6PGD) was studied. All the 11 mutations affect the structural gene of the Pgd locus: 3 semilethal mutations resulted in altered 6PGD molecules with decreased catalytic activities; the rest 8 lethals were "null" alleles characterized by mutant polypeptides capable of reacting with antisera against highly purified 6PGD. "Null" or low activity alleles for glucose-6-phosphate dehydrogenase induced by ethyl methanesulfonate were shown to be suppressores for the lethal mutations in the Pgd locus. A monocistronic type of organization of the Pgd locus is suggested taking into account the biochemical mechanism of suppression of the Pgd-lethals and their location in the structural gene coding for 6PGD.
Mol Gen Genet 1977 Jun 08
PMID:Investigations on the organization of genetic loci in Drosophila melanogaster: lethal mutations affecting 6-phosphogluconate dehydrogenase and their suppression. 40 44

Transversion mutations can be distinguished from transition mutations by the use of special tauII mutants of bacteriophage T4. Methyl methanesulfonate did not induce reversion of the tester mutants along transversion or transition pathways from A:T1 base pair sites, nor along transversion pathways from G:C base pair sites. Ethyl methanesulfonate and N-methyl-N-nitrosourea, however, induced both transversions and transitions at an A:T base pair site; no transversions were detected at G:C-sites. Mn++ induced transversions and transitions at both A:T-and G:C-sites. The influence of temperature-sensitive gene-43 DNA polymerase mutator and antimutator mutations on the reversion of the tauII tester mutants was measured: some gene-43 mutants differentially influenced different pathways of reversion. Studies of thymineless mutagenesis demonstrated A:T-site transversion mutations. A synergistic interaction between thymineless mutagenesis and the gene-43 mutator, tsL56, was used to demonstrate thymineless mutagenesis at one site where it was not detected in the presence of the wild type polymerase.
Mol Gen Genet 1975 Nov 03
PMID:Transversion mutagenesis in bacteriophage T4. 76 23


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