Disease relevance of Ethyl mesylate

• Mediation of EMS mutagenesis by an error-prone repair pathway in S. fradiae, rather than by direct mispairing as in Escherichia coli, suggests that the streptomycetes have evolved more efficient error-avoidance mechanisms than those commonly observed in the single-celled eubacteria [1].
• Reduced susceptibility to HIV-1 infection of ethyl-methanesulfonate-treated CEM subclones correlates with a blockade in their protein kinase C signaling pathway [2].
• Our results suggest that adenovirus particles and ethyl methane sulfonate induce mutations at the hpt locus of Hpt-13 cells through similar mechanisms [3].
• Strain GM3498, but not GM4408, exhibits a high frequency of spontaneous sister chromatid exchange, hypersensitivity to ethyl methanesulphonate and an anomalously low level of DNA ligase I activity [4].
• Molecular mechanisms in alkylation mutagenesis. Induced reversion of bacteriophage T4rII AP72 by ethyl methanesulphonate in relation to extent and mode of ethylation of purines in bacteriophage deoxyribonucleic acid [5].

Psychiatry related information on Ethyl mesylate

• Mitomycin C and ethyl methanesulphonate-induced sister-chromatid exchanges in lymphocytes from individuals with Alzheimer's pre-senile dementia [6].

High impact information on Ethyl mesylate

• In this note, I compare spontaneous forward mutant frequency with previously published revertant frequencies for one naturally occurring and six ethyl methanesulphonate-induced Adhl-deficient (Adh1-) alleles [7].
• T-DNA and ethyl-methane sulfonate mutagenesis allowed us to show that meiotic progression is altered in plants in which the AtSPO11-1 gene is disrupted [8].
• These cells were exposed to a mutagen, ethyl methane sulfonate, and variants that lost the capacity to bind PAC1 were isolated by fluorescence-activated cell sorting [9].
• High-density mutational spectra have been established for exon 3 of the gene encoding adenine phosphoribosyltransferase (APRT) of the Chinese hamster ovary (CHO) cell line derivative D422 and closely related and/or modified lines by using the mutagen ethyl methanesulfonate (EMS) [10].
• We investigated the effects of the well-known mutagenic agents ethyl methanesulfonate (EtMes), N-methyl-N-nitro-N-nitrosoguanidine (MNNG), and ICR-191 on colonies of the Chinese hamster ovary line CHO cultured on a semisolid substrate [11].

Chemical compound and disease context of Ethyl mesylate

• The induction of urothelial hyperplasia by methyl methanesulphonate and ethyl methanesulphonate [12].
• Twenty-six Acinetobacter calcoaceticus proline auxotrophs were isolated after ethyl methane sulfonate mutagenesis [13].
• The survival of phage resulting from in vitro packaging of DNA preexposed to various concentrations of methyl methane sulfonate or ethyl methane sulfonate closely paralleled the in vivo situation, in which intact phage were exposed to the alkylating agents [14].
• Strains V1 and V2 were studied in more detail and found to exhibit hypersensitivity to ethyl methanesulfonate (EMS), methyl methanesulfonate, and N-methyl-N'-nitro-N-nitrosoguanidine, but not to uv radiation [15].
• Treatment of HeLa cells with low doses of the carcinogens aflatoxin B1, methyl methanesulfonate (MMS) or ethyl methanesulfonate (EMS) increases the survival rate of UV-irradiated adenovirus 2 (ade2) [16].

Biological context of Ethyl mesylate

• Mitoses in EMS-treated cells were abnormal, involving multipolar mitotic spindles and elongated and/or incompletely condensed chromosomes [17].
• Flow cytometry revealed that EMS-treated EM9 cells underwent prolonged cell cycle arrest in G2, followed by entry into mitosis, micronucleation, and apoptosis [17].
• EM9 cells synchronized in G1 prior to EMS treatment entered mitosis 24-36 h after release from synchrony, approximately 12 h after untreated control cells [17].
• It was also found by this method that the number of DTr cells induced by a fixed concentration of EMS was not determined by the number of cell divisions during the expression time but by the period after exposure of the cells to EMS [18].
• We performed genetic screens in low white light-a threshold condition in which photomorphogenetic signaling pathways are only partially active-for ethyl methane sulfonate-generated mutants with altered developmental phenotypes [19].

Anatomical context of Ethyl mesylate

• This study describes the derivation of a series of mutants from the human leukemic cell line CEM using the frame shift mutagen Ethyl-methanesulfonate followed by negative selection with multiple treatments of OKT4A + C, and sorting into CD4-, CD4-dull, and CD4-intermediate mutants [20].
• Over 25 independently isolated variants were derived from an Abelson virus transformed pre- B cell line (R8) by mutagenesis with ethyl methane sulfonate or ethyl nitrosourea [21].
• We have initially used this system to demonstrate the generation of mutations by ethyl methanesulphonate (EMS) at a TaqI site in the aprt gene of Chinese hamster cells, and by u.v.-C irradiation at a TaqI site in the hprt gene of human fibroblasts [22].
• Dye coupling was abolished by treatment with either 1 mM octanol, 0.5 mM ethyl methanesulfonate (EMS), or cytoplasmic acidification, with coupling coefficients also being affected as each of these gap junction antagonists down-regulated the connexons [23].
• Both EMS and ENU induced mutations at high rates in post-meiotic germ cells, as indicated by the incidence of F1 progeny mosaic for the albino mutation [24].

Associations of Ethyl mesylate with other chemical compounds

• Since variants were ony found after ethyl methane sulfonate mutagenesis, the DNA alkylating agent appears to have promoted an epigenetic change in pituitary gene expression [25].
• Four bleomycin-sensitive mutants had increased sensitivities to killing by gamma-rays (2- to 3-fold), mitomycin C (2-fold), and ethyl methane sulfonate (4- to 5-fold), while six other mutants were resistant to these agents [26].
• All of the ethyl methane sulfonate- or nitrosomethylurea-generated mutants are missense mutations, as determined by sequencing of the ASP2 gene from the cytosolic aat2 mutants (aat2-1, aat2-2, aat2-4, and aat2-5) and the ASP5 gene from the chloroplastic aat3 mutants (aat3-1, aat3-2, and aat3-4) [27].
• Following mutagenesis with either ethyl methane sulfonate or nitrosoguanidine individual clones were tested at 34 degrees and 24 degrees for acetate-induced recombination [28].
• As expected for alkylation of guanine by EMS, >99% of mutations are G/C-to-A/T transitions [29].

Gene context of Ethyl mesylate

• 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 [30].
• We have employed the strategy of using ethyl methane sulfonate and taxol to perturb myofibril assembly to examine interactions critical for the addition of nebulin to the developing sarcomeres [31].
• Ethyl methanesulphonate (EMS) was able to mutate WP2 lexA [32].
• Deficiency of the enzyme adenine phosphoribosyltransferase (APRT) has been associated with hypersensitivity to the mutagenic effects of ethyl methanesulphonate (EMS) and 254 nm ultraviolet (UV) radiation in clone 707 of Friend mouse erythroleukaemia (FEL) cells [33].
• We have isolated mutants pasticcino belonging to 3 complementation groups (pas1, pas2, pas3) in the progeny of independent ethyl methane sulfonate and T-DNA mutagenized Arabidopsis thaliana plants [34].

Analytical, diagnostic and therapeutic context of Ethyl mesylate

• After treatment, the effective exposures were 2.5, 5.0, 7.5, 10.0, 15.0, and 30.0 mM EMS [35].
• Mammary carcinoma induced by oral administration of ethyl methanesulphonate. Determination of some of the parameters affecting tumor induction [36].
• Using gas chromatography we screened over 1,200 ethyl methane sulfonate (EMS)-mutagenized lines for alterations in the major A. thaliana wild-type stem cuticular chemicals [37].
• Tobacco seedlings were treated with EMS in the same manner as used for the comet assay and mutations were induced in the leaf primordia [38].
• Two V79 Chinese hamster sublines (V79-UL and V79-MZ) which differed markedly with respect to their spontaneous pattern of mutations at the HPRT locus were comparatively investigated in genotoxicity tests with ethyl methanesulphonate (EMS) [39].

References