Sobis H, Verstuyf A, Vandeputte M
Rega Institute for Medical Research, University of Leuven, Belgium.
Development. 1991 Jan;111(1):75-8. doi: 10.1242/dev.111.1.75.
Mutant mice deficient in glucose-6-phosphate dehydrogenase were used to induce teratomas. This enzyme is linked to the X chromosome, which can be inactivated in female embryo. The differences in the enzyme activity between yolk sac mesoderm and embryo versus yolk sac endoderm can be detected in female concepti by using appropriate crosses of wild-type and G6PD-deficient mice. Histochemical study showed that the dual cell population was observed in heterozygous embryos and in the embryomas derived from them. The teratomas derived from the corresponding yolk sac, however, were G6PD-positive from wild-type and G6PD-negative from homozygous enzyme-deficient mothers. We conclude that yolk-sac-derived teratomas are of endodermal origin because of the fact that the paternal X chromosome is inactivated in the yolk sac endoderm, whereas in the yolk sac mesoderm, as in the embryo, the inactivation is at random.
缺乏葡萄糖-6-磷酸脱氢酶的突变小鼠被用于诱导畸胎瘤。这种酶与X染色体相连,在雌性胚胎中X染色体会失活。通过使用野生型和G6PD缺陷型小鼠的适当杂交组合,可以在雌性孕体中检测到卵黄囊中层与胚胎和卵黄囊内胚层之间酶活性的差异。组织化学研究表明,在杂合子胚胎及其衍生的胚胎瘤中观察到了双细胞群体。然而,来自相应卵黄囊的畸胎瘤,野生型的为G6PD阳性,纯合酶缺陷型母亲的则为G6PD阴性。我们得出结论,源自卵黄囊的畸胎瘤是内胚层起源,因为父本X染色体在卵黄囊内胚层中失活,而在卵黄囊中层中,与胚胎一样,失活是随机的。