A review of the genetic effects of ethyl methanesulfonate

Sega, Gary A.

doi:10.1016/0165-1110(84)90007-1

Cited by 244 publications

(164 citation statements)

References 243 publications

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“…All eight cases of complementation are described in Table 1. The mutations were transitions at GC sites, as expected for the EMS mutagenesis (Sega 1984). No substitutions other than those reported in Table 1 were found.…”

Section: Resultssupporting

confidence: 67%

Why Molecular Chaperones Buffer Mutational Damage: A Case Study With a Yeast Hsp40/70 System

et al. 2006

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The malfunctioning of molecular chaperones may result in uncovering genetic variation. The molecular basis of this phenomenon remains largely unknown. Chaperones rescue proteins unfolded by environmental stresses and therefore they might also help to stabilize mutated proteins and thus mask damages. To test this hypothesis, we carried out a genomewide mutagenesis followed by a screen for mutations that were synthetically harmful when the RAC-Ssb1/2 cytosolic chaperones were inactive. Mutants with such a phenotype were found and mapped to single nucleotide substitutions. However, neither the genes identified nor the nature of genetic lesions implied that folding of the mutated proteins was being supported by the chaperones. In a second screen, we identified temperature-sensitive (ts) mutants, a phenotype indicative of structural instability of proteins. We tested these for an association with sensitivity to loss of chaperone activity but found no such correlation as might have been expected if the chaperones assisted the folding of mutant proteins. Thus, molecular chaperones can mask the negative effects of mutations but the mechanism of such buffering need not be direct. A plausible role of chaperones is to stabilize genetic networks, thus making them more tolerant to malfunctioning of their constituents.

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Section: Resultssupporting

confidence: 67%

Why Molecular Chaperones Buffer Mutational Damage: A Case Study With a Yeast Hsp40/70 System

et al. 2006

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“…Thus, the Mei1 m1Jcs point mutation occurred de novo during the course of the mutagenesis experiment. Interestingly, ethylmethanesulfonate (EMS) typically causes G-to-A or C-to-T transitions in ES cells (8), flies (13), and worms (14). It is possible that EMS induces A-to-T changes at a low frequency in ES cells as in Caenorhabditis elegans (Ϸ2% of all changes) (14).…”

Section: Resultsmentioning

confidence: 99%

Positional cloning and characterization of Mei1 , a vertebrate-specific gene required for normal meiotic chromosome synapsis in mice

Libby

Reinholdt

Schimenti

2003

Proc. Natl. Acad. Sci. U.S.A.

114

100

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The mouse meiotic mutant Mei1 was isolated in a screen for infertile mice descended from chemically mutagenized embryonic stem cells. Homozygotes of both sexes are sterile due to meiotic arrest caused by defects in chromosome synapsis. Notably, RAD51 protein does not load onto Mei1 mutant meiotic chromosomes, suggesting that there is a defect in either recombinational repair or the production of double-strand breaks (DSBs) that require such repair. Here, we show that treatment of mutant males with cisplatin restores RAD51 loading, suggesting that mutant spermatocytes have intact recombinational repair mechanisms. Levels of histone H2AX phosphorylation (␥H2AX) at leptonema are significantly reduced compared with wild-type controls but comparable to that seen in animals deficient for SPO11, the molecule required for catalyzing DSB formation during meiosis. These observations provide evidence that genetically programmed DSB induction is defective in Mei1 leptotene spermatocytes. We also report the positional cloning of Mei1, which encodes a product without significant homology to any known protein. Expressed almost exclusively in gonads, Mei1 has no apparent homologs in yeast, worms, or flies. However, Mei1 orthologs are present in the genomes of mammals, chickens, and zebrafish. Thus, Mei1 is required for vertebrate meiosis. To our knowledge, Mei1 is the first meiosis-specific mutation identified by forward genetic approaches in mammals.

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“…DNA polymorphism comparison between the BCNT002MT and BCNT002WT isolates showed different band patterns indicating changes in the DNA sequences. Normally EMS-induced mutations are evidenced by base-pair substitution (Sega 1984;Shiwa et al 2012). However, whether the DNA band patterns presented in BCNT002MT but not in BCNT002WT (or vice versa) might be involved (causal rather than incidental) with thermotolerant genes in B. bassiana is unknown, but of course it does not have to be the case.…”

Section: Discussionmentioning

confidence: 99%

“…Typically, EMS induces base-pair substitution, changing GC to AT and AT to CG, but sometimes EMS induces base-pair insertion or base-pair deletion (Sega 1984). Reports of EMS inducing mutagenesis in fungi include induced oxalic acid production in Metarhizium anisopliae (Leger 1999) and temperature-sensitive mutants in S. cerevisiae (Momose and Gregory 1998).…”

Section: Introductionmentioning

confidence: 99%

Development of thermotolerant isolates of Beauveria bassiana (Bals.-Criv.) Vuill. with ethyl methanesulfonate

Wongwanich

Cobelli

Boonchuay³

et al. 2018

Journal of Plant Protection Research

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Beauveria bassiana is an entomopathogenic fungus that is widely used in Thailand to control pest insects. However, the increasing temperature has influenced the insect control efficiency of the fungus. Therefore, determination of thermotolerant isolates of B. bassiana that can grow and remain pathogenic at higher temperatures than its current optimum temperature may be a better way to control pest insects in a high temperature environment. Three isolates of B. bassiana obtained from the Rice Department, Thailand were selected for mutagenesis using ethyl methanesulfonate (EMS) with subsequent screening at high temperatures (33 and 35°C). In addition, the recovery of fungal growth after exposure to a high temperature for a period of time (5-15 days) and then transferring to 25°C was evaluated. No isolates were found that grew at 35°C but one mutant isolate (BCNT002MT) produced larger diameter colonies and more spores than the corresponding wild type (WT) at 33°C. Growth and spore production of the BCNT002MT isolate were greater than its WT when incubated at 25°C for 14 days following exposure to 33°C for 7 days. In addition, the spore germination level (%) of BCNT002MT was significantly higher than its WT during culture at 25°C after prior exposure to 33°C for 5, 10 and 15 days. The pathogenicity against the brown planthopper, Nilaparvata lugens (Stål), of this mutant isolate was also prominent.

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A review of the genetic effects of ethyl methanesulfonate

Cited by 244 publications

References 243 publications

Why Molecular Chaperones Buffer Mutational Damage: A Case Study With a Yeast Hsp40/70 System

Why Molecular Chaperones Buffer Mutational Damage: A Case Study With a Yeast Hsp40/70 System

Positional cloning and characterization of Mei1 , a vertebrate-specific gene required for normal meiotic chromosome synapsis in mice

Development of thermotolerant isolates of Beauveria bassiana (Bals.-Criv.) Vuill. with ethyl methanesulfonate

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