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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over sixty EMS induced mutations affecting gene lamB, presumably the structural gene for the lambda receptor in Escherichia coli K12, were examined for growth of lambda host range mutants and effect of nonsense suppressors. By the first criterion the mutations could be grouped in three classes. Bacteria with class I mutations allow growth of lambda mutants with extended host range (noted lambdah) of the type already described (Appleyard, MacGregor and Baird, 1956). Bacteria with class II mutations allow growth of lambdah mutants with still more extended host range (noted lambdahh). No host range mutants of lambda could be found which would grow on bacteria with class III mutations. Using nonsense suppressors it was found that class I and II consist of missense mutations, while class III consists of nonsense mutations. Exceptions are likely to exist (especially in class III) but were not found among the mutations tested. These observations are briefly discussed in terms of outer membrane protein integration and of phage receptor interaction.
Mol Gen Genet 1976 May 07
PMID:lamB mutations in E. coli K12: growth of lambda host range mutants and effect of nonsense suppressors. 77 86

Mutagenesis of Escherichia coli K12 cells with ethyl methanesulfonate and selection of streptomycin-resistant mutants after a long delay for phenotypic expression allowed us to isolate new types of streptomycin-resistant ribosomes. Misreading patterns of the ribosomes in the presence of streptomycin revealed that most of the streptomycin-resistant mutants isolated under these conditions differed from the four classical types of streptomycin-resistant mutants studied and characterized by Strigini, P. and Gorini, L. (1970) J. Mol. Biol. 47, 517-530.
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PMID:New types of streptomycin-resistant mutants of Escherichia coli. 78 40

97 lethal and semilethal mutations were induced by ethyl methanesulfonate, nitrosomethyl urea and gamma-irradiation in the 2D3-F5 region of the X-chromosome of D. melanogaster. Approximately 1 per cent of the tested X-chromosomes carried a lethal in the 2D3-2F5 region. The mutation frequencies per band or DNA content in the region and the whole X-chromosome are equal. Complementation analysis revealed at least 10 functionally independent essential loci in this region including about 10 bands. The data presented in this study support the one band--one gene hypothesis. The Pgd locus coding for 6-phosphogluconate dehydrogenase (6PGD) is mapped in the 2D3 (OR 2D4) band. Isolation of 11 lethal or semilethal point mutations with null or reduced 6PGD activity shows that the Pgd locus is a vital one.
Mol Gen Genet 1975 Dec 01
PMID:Fine genetic structure of the 2D3-2F5 region of the X-chromosome of Drosophila melanogaster. 81 8

A temperature sensitive ligase allele of phage T4 reduced or eliminated HNO2 induced reversion of am mutants. Since at the temperatures used, the ligase mutant is defective in the repair of some types of lethal lesions (i.e., UV, MMS and EMS induced lesions) these results indicate that HNO2 mutagenesis may occur through a ligase dependent repair pathway. In contrast, 2AP induced mutation was not inhibited by mutants defective in the gene 30 ligase or in genes 32, 39, 41, 42, 44, 45, 46, 47, 49, 52, 56, 58-61 and v. This indicates that 2AP mutagenesis probably does not depend on a repair pathway in phage T4.
Mol Gen Genet 1976 Oct 18
PMID:The dependence of HNO2 mutagenesis in phage T4 on ligase and the lack of dependence of 2AP mutagenesis on repair functions. 97 60

A diploid yeast strain, D81, was constructed heterozygous for seven recessive markers linked on the left arm of chromosome VII to study the localization of induced mitotic crossing over. The mutagens used were carofur also called nifurprazinum (1-(5-nitro-2-furyl)-2-(6-amino-3-pyridazyl)-ethylene hydrochloride), diepoxybutane, ethylmethanesulfonate, nitrous acid and 1-nitrosoimidazolidinone-2. All agents induced high frequencies of mitotic crossing over at doses exerting only a low degree of killing. The distribution of recombinational events was compared for five intervals. The distribution pattern of spontaneous mitotic crossing over was different from all the patterns obtained after mutagenic treatments. Nitrous acid and diepoxybutane induced the same pattern, which was different from the patterns induced by carofur, EMS and 1-nitrosoimidazolidinone-2. The patterns induced by the latter three mutagens were again different amongst each other. Repeat experiments showed that the patterns induced by a given mutagen were reproducible. Tetrad analysis with a representative sample of segregants induced by diepoxybutane and carofur showed that the treatments actually induced mitotic crossing-over. The pattern of meiotic recombinational events was different from those of spontaneous and mutagen induced mitotic recombination. Inducibility of mitotic crossing-over was low at the proximal and distal ends of the chromosome arm and highest in the middle. Each interval showed a different response to those mutagens that differed in their patterns of induced mitotic crossing over. The observed mutagen specific effects are considered as an indication of mutagen specificity. No plausible explanation for mutagen specificity could be given. However, the data presented reveal the same situation as found in induction of chromosome breaks, as reported by other authors. Apparently, mutagen specificity is quite a general phenomenon even for genetic effects in larger intervals of a chromosome.
Mol Gen Genet 1975 Aug 27
PMID:Mutagen specificity in the induction of mitotic crossing-over in Saccharomyces cerevisiae. 110 40

A mitotic "recombination-competent state" inducible by x-irradiation is thought to exist in yeast. We sought evidence for such a process in mammalian cells by examining the occurrence of mutations at unlinked loci in clones derived from a human lymphoblast cell line. A total of 169 independent clones that arose spontaneously or after exposure to x-rays or ethyl methanesulfonate were selected for new somatic mutations at the thymidine kinase gene on chromosome 17q. They were subsequently screened for coincident mutations by use of variable-number-of-tandem-repeat probes located on different chromosomes. Three coincident mutations were positively identified by Southern analysis on chromosomes 7 and 14; they included one that produced a new allele and two that caused loss of allele heterozygosity. Densitometric analysis of the latter two indicated the presence of two copies of the remaining allele. Several possible coincident genetic events were also observed on chromosome 17. These findings revealed a coincident mutant fraction of about 10(-2)/cell, whereas the expected mutation fraction at these loci is less than 10(-4)/cell. These results may thus provide the first molecular evidence that a "global" mutational process capable of inducing genetic instability exists in mammalian cells.
Mol Carcinog 1992
PMID:Evidence for coincident mutations in human lymphoblast clones selected for functional loss of a thymidine kinase gene. 149 3

The base alterations induced by four alkylating agents, methyl methanesulfonate (MMS), ethyl methanesulfonate (EMS), N-nitroso-N-methylurea (MNU), and N-nitroso-N-ethylurea (ENU), have been determined at the URA3 locus in the yeast Saccharomyces cerevisiae. The mutagen treatment was carried out on yeast cells in the logarithmic phase of growth. The mutants were selected by their resistance to 7.3 mM-5-fluoroorotic acid at pH 3.8. DNA sequence analysis was carried out by the dideoxy chain termination method. The alkylating agents were selected for their widely differing Swain-Scott substrate constants (s values), which are as follows: MMS, s = 0.83; EMS, s = 0.67; MNU, s = 0.42; ENU, s = 0.26. A higher s value is correlated with a higher ratio of 7-alkylguanine to O6-alkylguanine in native DNA in vitro. 125 forward mutations from URA3----ura3 were sequenced with marked differences in the mutational spectra being observed as the s value changed. Five hotspots were recorded for the four alkylating agents. They were all G.C----A.T transition mutations. There was one common hotspot for all of them; there were two additional ones for the two ethylating agents (ENU and EMS) and two different ones for MNU. Four of the five hotspots have the 5'-GG-3' sequence with the 3'-guanine mutated. It was seen that MMS, which has the highest Swain-Scott substrate constant, yielded the widest array of mutational types. As the substrate constants decreased, the types of mutations became more and more restricted to the G.C----A.T transitions and the A.T----T.A transversions. The transitions are consistent with the concept that mutations arise from O6-alkylation of guanine and alkylation of thymine. The transversions are consistent with the notion of N1-alkylation of adenosine or adenylic acid.
J Mol Biol 1992 Feb 05
PMID:Base alterations in yeast induced by alkylating agents with differing Swain-Scott substrate constants. 154 9

The subject of this study is the organization of essential genes in the 2 map-unit unc-22 IV region of the Caenorhabditis elegans genome. With the goal of achieving mutational saturation of essential genes in this region, 6491 chromosomes mutagenized with ethyl methanesulfonate (EMS) were screened for the presence of lethal mutations in the unc-22 region. The genetic analysis of 21 lethal mutations in the unc-22 region resulted in the identification of 6 new essential genes, making a total of 36 characterized to date. A minimum of 49 essential genes are estimated to lie in this region. A set of seven formaldehyde-induced deficiencies of unc-22 and surrounding loci were isolated to facilitate the positioning of essential genes on the genetic and physical maps. In order to study essential genes at the molecular level, our approach was to rescue lethal mutations by the injection of genomic DNA in the form of cosmid clones into the germ-line of balanced heterozygotes carrying a lethal mutation. The cosmid clones containing let-56 and let-653 were identified by this method.
Mol Gen Genet 1992 Mar
PMID:Genetic analysis and complementation by germ-line transformation of lethal mutations in the unc-22 IV region of Caenorhabditis elegans. 155 9

In this work we report on the isolation of an Escherichia coli K-12 mutation, which confers a high sensitivity to bacteria cells to mutagenesis by simple monofunctional alkylating agents. The mutation emerged spontaneously from a bacterial strain that already proved useful in various mutagenicity studies. By monitoring the influence of such a mutation on the frequency of induced mutation by ethylating (EMS, DES, ENU, ENNG) vs. methylating (MMS, DMS, MNU, MNNG) compounds, and on the in vivo repair capacity for different alkyl-DNA lesions (O6-alkG, N7-alkG, N3-meA), we conclude that the mutation should affect the gene (ogt) that encodes constitutive DNA repair alkyltransferase (ATase). Thus in the presence of ada, differences in mutagenicity were observed only with ethylating agents; the sensitization of cells to both the ethylating and methylating partners requiring, by contrast, the absence of the ada protein. These results support the reported in vitro substrate specificities for both ogt and ada ATases. The parental cells exhibited biphasic dose-response curves in accordance with the idea of low basal level saturation attributed to the uninducible ogt ATase. Deficient bacterial derivatives showed, by contrast, linear mutation induction responses. The in vivo removal of alkylated bases from DNA was measured in bacterial strains deficient in the excision repair pathway (delta uvrB) and unable to induce the adaptive response (ada::Tn10). The very low initial levels for O6-meG and O6-etG (1.1 and 0.2 molecules per cell, respectively) were readily repaired by the parental cells but remained unchanged in the hypermutable derivatives. This result suggests that in the absence of nucleotide excision repair and of the adaptive response, no alternative pathway, other than ogt, is available for the repair of the major mutagenic lesion, O6-alkG, at least during the first 4 hours after alkylation. Comparatively, no differences were found in the capacity to repair the major lethal adduct, N3-meA, in agreement with the fact that no effect on cell survival was detected. In conclusion, we propose that the biological significance of the ogt protein relies mainly on its ability to prevent mutagenesis by low levels of bulkier ethylation products (especially in the absence of uvr excision repair.(ABSTRACT TRUNCATED AT 400 WORDS)
Environ Mol Mutagen 1992
PMID:Mutagenesis and DNA repair for alkylation damages in Escherichia coli K-12. 160 Sep 55

We have found that Arabidopsis thaliana is susceptible to infection with a crucifer strain of tobacco mosaic virus (TMV-Cg); the coat protein of TMV-Cg accumulated to a high level in uninoculated rosette leaves several days after inoculation. As a first step in the search for host-coded factors that are involved in virus multiplication, we isolated mutants of A. thaliana in which the accumulation of TMV-Cg coat protein was reduced to low levels. Of 6000 M2 plants descended from ethyl methanesulfonate-treated seeds, two such lines (PD114 and PD378) were isolated. Genetic analyses suggested that the PD114 phenotype was caused by a single nuclear recessive mutation, and that PD114 and PD378 belonged to the same complementation group. The coat protein accumulation of a tomato strain of TMV (TMV-L) was also reduced in PD114 plants compared to that in the wild-type plants. In contrast, PD114 plants infected with turnip crinkle or turnip yellow mosaic viruses, which belong to taxonomic groups other than Tobamovirus, expressed similar levels of these coat proteins as did infected wild-type plants.
Mol Gen Genet 1991 Nov
PMID:Isolation of mutants of Arabidopsis thaliana in which accumulation of tobacco mosaic virus coat protein is reduced to low levels. 174 39


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