HGPRT activity changes in preimplantation mouse embryos (original) (raw)

Nature volume 274, pages 503–504 (1978)Cite this article

Abstract

TO compensate for unequal doses of genes on the X chromosomes of males and females, one of the X chromosomes in the somatic cells of mammalian females is inactive1. This inactivation occurs early in development, although the exact time is unknown2. Before X-chromosome inactivation, and in the absence of other dosage compensating mechanisms, female embryos with two X chromosomes would be expected to have twice as much activity for an X-linked enzyme as male embryos with only one X chromosome. In a litter with approximately an equal number of male and female embryos, the distribution of enzyme activity should have two equal-sized peaks separated by a factor of two. The change from a bimodal to unimodal distribution would indicate that X-chromosome inactivation had occurred. Early in development, the X-linked enzymes _α_-galactosidase (_α_-gal)3 and hypoxanthine guanine phosphoribosyltransferase (HGPRT)4,5 are both derived from embryonic gene activity. _α_-gal was found to have a bimodal distribution at the morula stage3. For HGPRT, Monk and Kathuria6 found no bimodality at either the eight-cell or blastocyst stages, however further analysis revealed bimodality at certain stages7. Epstein _et al._8 have found that females have twice as much HGPRT activity as males in early blastocysts. We present here evidence for the activity of both the maternal and paternal X chromosomes by the eight-cell stage, with inactivation initiated at blastulation.

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Authors and Affiliations

  1. Departments of Genetics and Medicine, University of Washington, Seattle, Washington, 98195
    PAUL G. KRATZER & STANLEY M. GARTLER

Authors

  1. PAUL G. KRATZER
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  2. STANLEY M. GARTLER
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KRATZER, P., GARTLER, S. HGPRT activity changes in preimplantation mouse embryos.Nature 274, 503–504 (1978). https://doi.org/10.1038/274503a0

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