The steroid sulfatase locus on structurally abnormal inactive X chromosomes is expressed

The steroid sulfatase locus on structurally abnormal inactive X chromosomes is expressed

In mammalian somatic cells, sex-chromosome dosage compensation is achieved by random inactivation of one of the two X chromosomes. The Xg blood group antigen (Xg) and steroid sulfatase (STS) loci on the distal end of the short arm of the X chromosome have been shown to escape this inactivation. Howe...

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Bibliographic Details
Published in:American journal of human genetics Vol. 36; no. 5; pp. 979 - 986
Main Authors: IMMKEN, L, MOHANDAS, T, SPARKES, R. S, SHARPIRO, L. J
Format: Journal Article
Language:English
Published: Chicago, IL University of Chicago Press 01-09-1984
Subjects:
Animals
Biological and medical sciences
Blood Group Antigens - genetics
Cell Fusion
Cell Line
Chromosome Banding
Chromosome Mapping
Dermatology
Dosage Compensation, Genetic
Female
Genetic Markers
Hereditary diseases of the skin. Congenital diseases of the skin. Haemangioma of the skin, of mucosae and of soft tissue
Humans
Karyotyping
Medical sciences
Mice
Steryl-Sulfatase
Sulfatases - genetics
X Chromosome
Chromosomal aberration
Human
Sex linked character
Skin disease
Hybrid cell
Abnormal X chromosome
Enzyme
Deficiency
Rodentia
Somatic cell
Metabolic diseases
Gene expression
Inactivation
Ichthyosis
Vertebrata
Mammalia
Mouse
Abnormal chromosome
Sterol-sulfatase
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Description
Summary:In mammalian somatic cells, sex-chromosome dosage compensation is achieved by random inactivation of one of the two X chromosomes. The Xg blood group antigen (Xg) and steroid sulfatase (STS) loci on the distal end of the short arm of the X chromosome have been shown to escape this inactivation. However, it has been reported that on structurally abnormal inactive X chromosomes Xg and STS are inactivated. This discrepancy requires further consideration since whatever process accounts for the lack of inactivation of these loci on structurally normal, inactive X chromosomes might be anticipated to be operative on structurally abnormal, inactive X chromosomes. To investigate this issue, we examined the expression of STS activity in mouse-human somatic-cell hybrids retaining two different, deleted, inactive human X chromosomes. These studies provide evidence for lack of inactivation of STS on structurally abnormal, inactive X chromosomes.
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ISSN:0002-9297
1537-6605