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Mutants as Tools for the Analytical Dissection of Cell Differentiation in Physcomitrella Patens Gametophytes
Published in R. N. Chopra, Satish C. Bhatla, Bryophyte Development: Physiology and Biochemistry, 2019
In both cases, developmentally abnormal mutants have proven to be immensely valuable analytical tools. In most instances the mutants have been induced by treating haploid spores with a chemical mutagen, usually N-methyl-N′-nitro-N-nitrosoguanidine (NTG) or ethyl methanesulfonate (EMS), although occasionally other mutagens, including ultraviolet (UV) light, have been utilized.3,4,12,14,22,30 In the future it may prove more convenient to induce developmental mutations by somatic mutagenesis, a technique recently perfected in P. patens.7,22,31
Mutagenic Consequences Of Chemical Reaction with DNA
Published in Philip L. Grover, Chemical Carcinogens and DNA, 2019
The reason the author would suggest for these discrepancies is that, although crosslinks are of major significance in determining survival, it is the nature of the monoad-duct which primarily determines mutagenicity. Nitrogen mustard is considered to be a classical SN2-type alkylating agent and as such would be expected to resemble methyl methanesulfonate rather than ethyl methanesulfonate as a mutagen. It should therefore be rather weakly mutagenic, and the mutations would be expected to arise through error-prone repair. Surprisingly, experiments by W. J. Muriel and the author show that nitrogen mustard mutagenesis is entirely independent of error-prone repair (Table 3), since it occurs equally readily in a lexA strain of E. coli. This suggests that nitrogen mustard probably alkylates the O6 position of guanine, and as such causes errors in replication. If a proportion of monoadducts are of this type, they will be highly mutagenic. Table 3 suggests that they are subject to uvr-dependent excision.
Genomic Instability During Aging of Postmitotic Mammalian Cells
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
If chromosomal aberrations are the basis for radiation shortening the life span, then any agent capable of inducing chromosomal aberrations should cause the same effect. The ability of nitrogen mustard and other radiomimetic compounds to bring on chromosomal abnormalities, such as breaks and rearrangements, is just one of a number of properties that they share in common with radiation.14 Some radiomimetic agents, when given in fractional doses, were reported to shorten the life span,108–110 but many experiments demonstrated that nitrogen mustard did not decrease life span when given either as massive single doses or as multiple smaller doses split over the first half of the animals’ life span.12,81,83 Likewise, ethyl methane sulfonate, a known mutagen, did not decrease life span, but greatly increased tumor incidence at death.15 However, the rate of accumulation of chromosomal aberrations of the nitrogen mustard-treated mice was only slightly higher than control mice.12 This result suggests that significant repair of nitrogen mustard-induced lesions took place in the interphase liver cells.
Development and characterization of gamma ray and EMS induced mutants for powdery mildew resistance in blackgram
Published in International Journal of Radiation Biology, 2023
Murugesan Tamilzharasi, Dharmalingam Kumaresan, Venkatesan Thiruvengadam, Jegadeesan Souframanien, T. K. S. Latha, N. Manikanda Boopathi, Palaniappan Jayamani
Mutations can be induced artificially by using physical (X-rays, gamma rays, and neutrons) and chemical (ethyl methanesulfonate) mutagens (Khursheed et al. 2021). Among the physical mutagens, X-rays and gamma ray (ionizing radiations) are widely used, since they produce point mutations and deletions. Chemical mutagens are easy to use and produce high mutation frequency (Ibrahim et al. 2018). The commonly used chemical mutagen is ethyl methanesulfonate (EMS) and it creates single nucleotide polymorphism (SNP). Any planting materials such as seeds, cuttings, pollen, or tissue-cultured calli can be used as source material for inducing mutation (Melsen et al. 2021). The combined use of ionizing radiation and chemical mutagen results in a significant effect on the genome (Laskar et al. 2015; Tiliouine et al. 2018; Abaza et al. 2020) and Usharani and Kumar (2015) also observed a synergistic effect and increased mutation rate on combining gamma ray and EMS in blackgram.
Developments in drug design strategies for bromodomain protein inhibitors to target Plasmodium falciparum parasites
Published in Expert Opinion on Drug Discovery, 2020
Hanh H. T. Nguyen, Lee M. Yeoh, Scott A. Chisholm, Michael F. Duffy
Targets of putative BRD inhibitors can also be validated by generating parasites with increased resistance to the compound and identifying the associated polymorphisms [100]. These parasites can be generated by exposure to sublethal concentrations of the compound (usually 3- to 10-fold IC50) until parasites recover [64], or by increasing the concentration of the compound over a prolonged period of time until resistance is achieved; this can take months to years [101,102]. To expedite this method, parasites can be treated with mutagenic agents such as ethyl methanesulfonate to increase sequence heterogeneity in the genome, which will undergo selection after treatment with the compound of interest [103]. These approaches can identify the residues within the protein targets that are bound by the hit compounds but can also identify components of a related pathway or other off-target genes that have mutated and compensated for the effect of drugs. Therefore, the specificity of target proteins or residues identified must be validated through in vitro assays or reverse genetic approaches.
Pre-Exposure to Chronic Unpredictable Stress Suppresses the Chemopreventive Potential of Aloe Vera (Av) Leaf Gel Against 7,12-Dimethylbenz(a)anthracene (DMBA) Induced Carcinogenesis
Published in Nutrition and Cancer, 2019
Nida Suhail, Nayeem Bilal, Shirin Hasan, Naheed Banu
DMBA + TPA in the present study was shown to induce DNA damage in lymphocytes and skin cells of mice, measured by alkaline comet assay in terms of increased DNA tail length. However, Av gel application for the entire experimental period significantly decreased the DMBA + TPA induced DNA damage in the two types of cells studied. A plausible reason for this may be that the components present in the aloe gel inhibited the binding of the carcinogen to the cells and thus prevented the formation of potential cancer-initiating carcinogen-DNA adducts. Aloe has been shown to exhibit antigenotoxic effects against mutagenicity induced by alkylating agent ethyl methanesulfonate (39). A polysaccharide fraction of aloe gel and aloe extract is found to inhibit the binding of benzopyrene to primary rat hepatocytes and thus is shown to prevent the formation of potential cancer-initiating benzopyrene DNA adducts (40). In another study, aloe gel caused an induction of glutathione-S-transferase and inhibition of tumor promoting effects of TPA (41), thus suggesting a possible benefit of using aloe gel and aloe extract in cancer chemoprevention. These properties allow Av gel to preserve macromolecules including DNA, protein, and lipid from oxidative damage resulting from chemical carcinogen exposure.