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Biomedical subjects

B R Migeon

Publications and source records attributed to B R Migeon.

At least 109 records · Page 6Linked to original sources
PubMed1975

Stability of X chromosomal inactivation in human somatic cells transformed by SV-40.

Clones of fibroblasts from a G6PD A heterozygote transformed with SV-40 did not express the G6PD silent allele in the transformed heteroploid cultures. In addition, transformed fibroblasts from a woman heterozygous for both G6PD A and HGPRT deficiency, subjected to selective pressure, did not reveal a single cell expressing either silent allele. Since the incidence of sex chromatin was significantly lower in these cells after transformation, it is likely that the loss of sex chromatin reflects the loss of the inactive X-chromosome at an early stage following transformation.

Aneuploidy↗
PubMed1975

D-valine as a selective agent for normal human and rodent epithelial cells in culture.

A nutrient medium has been developed to enable the growth of normal epithelial cells while selectively inhibiting fibroblast proliferation. In this medium, D-valine is substituted for L-valine; and only those cells containing D-amino acid oxidase can convert the D-amino acid into its essential L-enantiomer. The ability to select for cells with this enzyme has enabled us to maintain epithelial cell populations free from fibroblast overgrowth. The presence of D-amino acid oxidase has been histochemically confirmed in the epithelial cells selected from renal cell suspensions and explants. The ability to proliferate in the selective medium is transmitted to the clonal progeny of these cells. Moreover, epithelial cell proliferation of this medium indicates the presence of D-amino acid oxidase, which we have detected in tissues where it had not previously been reported-fetal human kidney, lung, and cord. Fibroblasts will not grow in the selective medium, but will proliferate normally if the product of the D-amino acid oxidase reaction is supplied.

Animals↗
PubMed1975

Locus on human X chromosome for dihydrotestosterone receptor and androgen insensitivity.

We have studied androgen binding characteristics of cells for androgen insensitivity from an obligate heterozygote, who is the mother of three male pseudohermaphrodites with dihydrotestosterone (17beta-hydroxy-5alpha-androstan-3-one) receptor deficiency. Specific dihydrotestosterone binding by skin fibroblasts from her wrist and pubis is within the normal range and indicates that androgen insensitivity is X-linked in man and is therefore homologous to the tfm locus in the mouse. A significant population of clones from the heterozygote has deficient receptor activity, and this finding is compatible with inactivation of one X-linked allele at this locus. Our results indicate the presence of a gene on the human X chromosome that is essential for normal male sexual differentiation and provide further evidence for homology between X chromosomes of all mammals.

Binding Sites↗
PubMed1975

Evidence for the inactivation of an X chromosome early in the development of the human female.

Studies of somatic tissues and cultured cells, including fibroblast clones, from human embryos heterozygous for the electrophoretic variants of glucose-6-phosphate dehydrogenase confirm that one X chromosome is inactivated very early in embryonic development and indicate that X inactivation has occurred in the majority of cells from a variety of tissues at least by 5 weeks from conception.

Blood Protein Electrophoresis↗
PubMed1974

Isolation and analysis of somatic hybrids derived from two human diploid cells.

Lesch-Nyhan fibroblasts and normal human leukocytes with different glucose-6-phosphate dehydrogenase genotypes were fused by Sendai virus. Clones were isolated on the basis of their resistance to a medium containing hypoxanthine, amethopterin, and thymidine and ability to proliferate in monolayer culture. These mononuclear cells (1) incorporated [(3)H]hypoxanthine, (2) expressed the glucose-6-phosphate dehydrogenase heteropolymer, and (3) were polyploid. Therefore, hybrids can originate from the fusion of two diploid human cells. X chromosome inactivation did not occur in these hybrid cells of male origin. The hybrids expressed both parental genomes and exhibited the senescence and contact feeding characteristic of the human skin fibroblast.

Autoradiography↗
PubMed1970

Genetic inactivation of the alpha-galactosidase locus in carriers of Fabry's disease.

Skin fibroblasts from a patient with Fabry's disease showed deficient activity of alpha-galactosidase. Fibroblasts from his mother and sister had two distinct clonal populations, one with enzymatic activity and the other enzyme deficient. This provides evidence of genetic inactivation at the alpha-galactosidase locus and makes possible the detection of carriers of Fabry's disease even when the enzymatic activity in their leukocytes and uncloned fibroblasts is within the range of controls.

Adolescent↗