Immken L, Mohandas T, Sparkes R S, Shapiro L J
Am J Hum Genet. 1984 Sep;36(5):979-86.
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.
在哺乳动物体细胞中，通过两条X染色体中的一条随机失活来实现性染色体剂量补偿。X染色体短臂远端的Xg血型抗原（Xg）和类固醇硫酸酯酶（STS）基因座已被证明可逃避这种失活。然而，据报道，在结构异常的失活X染色体上，Xg和STS会被失活。这种差异需要进一步考虑，因为无论何种过程导致这些基因座在结构正常的失活X染色体上未被失活，都可能预期在结构异常的失活X染色体上也起作用。为了研究这个问题，我们检测了保留两条不同的、缺失的、失活的人类X染色体的小鼠-人类体细胞杂种中STS活性的表达。这些研究为STS在结构异常的失活X染色体上未被失活提供了证据。
