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. 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.
D000818:Animals; D001789:Blood Group Antigens / Q000235:genetics; D002459:Cell Fusion; D002460:Cell Line; D002871:Chromosome Banding; D002874:Chromosome Mapping; D004303:Dosage Compensation, Genetic; D005260:Female; D005819:Genetic Markers; D006801:Humans; D007621:Karyotyping; D051379:Mice; D043266:Steryl-Sulfatase; D013429:Sulfatases / Q000235:genetics*; D014960:X Chromosome
D001789:Blood Group Antigens; D005819:Genetic Markers; D013429:Sulfatases; D043266:Steryl-Sulfatase