The Experts below are selected from a list of 69 Experts worldwide ranked by ideXlab platform

Yoshio Sano - One of the best experts on this subject based on the ideXlab platform.

  • mutagenicity of o diazoacetyl l serine azaserine and 6 diazo 5 oxo l norleucine don in a soybean test system
    Mutation Research\ genetic Toxicology, 1995
    Co-Authors: Yoshinobu Katoh, Masahiko Maekawa, Yoshio Sano
    Abstract:

    Abstract The mutagenicity of O- diazocetyl- l -serine (azaserine) and 6-diazo-5-oxo- l -norleucine (DON), glutamine analogues, were assayed in heterozygous soybean plants (Y11y11), according to the appearance of mutational spots (yellow, dark green and twin) on the leaves. The mutagenicity of azaserine was detected at 0.1 mg/ml, and that of DON, at 0.05 mg/ml. DON was strongly cytotoxic at doses exceeding 0.1 mg/ml. After azaserine and DON treatment, large spots which occupied more than half the leaflet were found in the first and second compound leaves. The glutamine analogues increased the frequency of yellow spots much more than dark green spots or twin spots. Light green spots were observed on y11y11 plants. Azaserine and DON induce Somatic Crossing over, point mutation and segmental loss as major effects.

  • Effects of 5-azacytidine on Somatic mutation in a soybean test system.
    Mutation research, 1993
    Co-Authors: Yoshinobu Katoh, Masahiko Maekawa, Yoshio Sano
    Abstract:

    Abstract The mutagenic activity of 5-azacytidine (azaC) was assayed in heterozygous soybean plants (Yllyll), according to the appearance of mutational spots (yellow, dark green and twin) on the leaves. When soybean seeds were treated with azaC at 10–100 μg/ml, azaC was found to be significantly mutagenic and to exert heritable effects in the soybean test system. Treatment with azaC increased the frequency of twin spots on the leaves. AzaC would thus appear to cause Somatic Crossing over as its major effect.

Yoshinobu Katoh - One of the best experts on this subject based on the ideXlab platform.

  • mutagenicity of o diazoacetyl l serine azaserine and 6 diazo 5 oxo l norleucine don in a soybean test system
    Mutation Research\ genetic Toxicology, 1995
    Co-Authors: Yoshinobu Katoh, Masahiko Maekawa, Yoshio Sano
    Abstract:

    Abstract The mutagenicity of O- diazocetyl- l -serine (azaserine) and 6-diazo-5-oxo- l -norleucine (DON), glutamine analogues, were assayed in heterozygous soybean plants (Y11y11), according to the appearance of mutational spots (yellow, dark green and twin) on the leaves. The mutagenicity of azaserine was detected at 0.1 mg/ml, and that of DON, at 0.05 mg/ml. DON was strongly cytotoxic at doses exceeding 0.1 mg/ml. After azaserine and DON treatment, large spots which occupied more than half the leaflet were found in the first and second compound leaves. The glutamine analogues increased the frequency of yellow spots much more than dark green spots or twin spots. Light green spots were observed on y11y11 plants. Azaserine and DON induce Somatic Crossing over, point mutation and segmental loss as major effects.

  • Effects of 5-azacytidine on Somatic mutation in a soybean test system.
    Mutation research, 1993
    Co-Authors: Yoshinobu Katoh, Masahiko Maekawa, Yoshio Sano
    Abstract:

    Abstract The mutagenic activity of 5-azacytidine (azaC) was assayed in heterozygous soybean plants (Yllyll), according to the appearance of mutational spots (yellow, dark green and twin) on the leaves. When soybean seeds were treated with azaC at 10–100 μg/ml, azaC was found to be significantly mutagenic and to exert heritable effects in the soybean test system. Treatment with azaC increased the frequency of twin spots on the leaves. AzaC would thus appear to cause Somatic Crossing over as its major effect.

Masahiko Maekawa - One of the best experts on this subject based on the ideXlab platform.

  • mutagenicity of o diazoacetyl l serine azaserine and 6 diazo 5 oxo l norleucine don in a soybean test system
    Mutation Research\ genetic Toxicology, 1995
    Co-Authors: Yoshinobu Katoh, Masahiko Maekawa, Yoshio Sano
    Abstract:

    Abstract The mutagenicity of O- diazocetyl- l -serine (azaserine) and 6-diazo-5-oxo- l -norleucine (DON), glutamine analogues, were assayed in heterozygous soybean plants (Y11y11), according to the appearance of mutational spots (yellow, dark green and twin) on the leaves. The mutagenicity of azaserine was detected at 0.1 mg/ml, and that of DON, at 0.05 mg/ml. DON was strongly cytotoxic at doses exceeding 0.1 mg/ml. After azaserine and DON treatment, large spots which occupied more than half the leaflet were found in the first and second compound leaves. The glutamine analogues increased the frequency of yellow spots much more than dark green spots or twin spots. Light green spots were observed on y11y11 plants. Azaserine and DON induce Somatic Crossing over, point mutation and segmental loss as major effects.

  • Effects of 5-azacytidine on Somatic mutation in a soybean test system.
    Mutation research, 1993
    Co-Authors: Yoshinobu Katoh, Masahiko Maekawa, Yoshio Sano
    Abstract:

    Abstract The mutagenic activity of 5-azacytidine (azaC) was assayed in heterozygous soybean plants (Yllyll), according to the appearance of mutational spots (yellow, dark green and twin) on the leaves. When soybean seeds were treated with azaC at 10–100 μg/ml, azaC was found to be significantly mutagenic and to exert heritable effects in the soybean test system. Treatment with azaC increased the frequency of twin spots on the leaves. AzaC would thus appear to cause Somatic Crossing over as its major effect.

James A. Birchler - One of the best experts on this subject based on the ideXlab platform.

  • Curt Stern on Somatic Crossing over.
    Genetics, 2016
    Co-Authors: James A. Birchler
    Abstract:

    ![Figure][1] In the mid-1930s, Curt Stern was investigating why certain Drosophila mutants develop mosaic patches with different body bristle phenotypes, when he noticed a recurring pattern. In one particular cross, the offspring sometimes carried areas with one recessive phenotype (yellowish

Gerd Scherer - One of the best experts on this subject based on the ideXlab platform.

  • A homozygous nonsense mutation in SOX9 in the dominant disorder campomelic dysplasia: a case of mitotic gene conversion
    Human Genetics, 2005
    Co-Authors: Michael V. Zaragoza, Mara Gaudette, Ulrike Dohrmann, Gerd Scherer
    Abstract:

    Campomelic dysplasia (CD; MIM 114290), an autosomal dominant skeletal malformation syndrome with XY sex reversal, is caused by heterozygous de novo mutations in and around the SOX9 gene on 17q. We report a patient with typical signs of CD, including sex reversal, who was, surprisingly, homozygous for the nonsense mutation Y440X. Since neither parent carried the Y440X mutation, possible mechanisms explaining the homozygous situation were a de novo mutation followed by uniparental isodisomy, Somatic Crossing over, or gene conversion. As the patient was heterozygous for six microsatellite markers flanking SOX9 , uniparental isodisomy and Somatic Crossing over were excluded. Analysis of intragenic single-nucleotide polymorphisms suggested that the homozygous mutation arose by a mitotic gene conversion event involving exchange of at least 440 nucleotides and at most 2,208 nucleotides between a de novo mutant maternal allele and a wild-type paternal allele. Analysis of cloned alleles showed that homozygous mutant cells constituted about 80% of the leukocyte cell population of the patient, whereas about 20% were heterozygous mutant cells. Heterozygous Y440X mutations, previously described in three CD cases, have been identified in seven additional cases, thus constituting the most frequent recurrent mutations in SOX9 . These patients frequently have a milder phenotype with longer survival, possibly because of the retention of some transactivation activity of the mutant protein on SOX9 target genes, as shown by cell transfection experiments. The fact that the patient survived for 3 months may thus be explained by homozygosity for a hypomorphic rather than a complete loss-of-function allele, in combination with Somatic mosaicism. This is, to our knowledge, the first report of mitotic gene conversion of a wild-type allele by a de novo mutant allele in humans.