Molecular Human Reproduction, Vol 3, 77-80, Copyright © 1997 by Oxford University Press
T Goto, E Wright and M Monk
Dosage compensation for X-chromosome-linked genes between male and female
mammals occurs by inactivation of one of the two X chromosomes in the
female. In somatic cells, either the paternal or the maternal X chromosome
is randomly inactivated in a given cell. In contrast, in the
extra-embryonic tissues of mice, the paternally-derived X chromosome is
preferentially inactivated. The evidence for paternal X-chromosome
inactivation in humans is controversial and remains to be clarified. In
this study, we have developed a sensitive polymerase chain reaction (PCR)
technique to investigate the methylation pattern of the X-linked androgen
receptor (AR) gene. The 5' CpG island of this gene is methylated on the
inactive X chromosome and hypomethylated on the active X chromosome in
somatic cells. The paternal and the maternal alleles of the AR gene may be
distinguished by a polymorphism in the number of CAG triplet repeats within
the CpG island. As a source of human extra-embryonic tissue, we used
chorionic villus (CV) samples from female conceptuses of 10-12 weeks
gestation. From a tiny branch of a CV sample, two distinct cell lineages,
the trophoblastic and mesodermal lineages, were dissected apart by trypsin
digestion and micromanipulation and DNA was extracted separately from these
purified tissues. Digestion of the DNA with the methylation-sensitive
restriction enzyme, Hpall, followed by PCR amplification revealed that the
paternal allele is preferentially methylated in trophoblastic cells, but
not in mesodermal cells. These results strongly suggest that the paternal X
chromosome is preferentially inactivated in the human extra-embryonic
tissues early in development.
JOURNAL ARTICLE
Paternal X-chromosome inactivation in human trophoblastic cells
Molecular Embryology Unit, Institute of Child Health, London, UK.
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