Letter | Published:

HGPRT activity changes in preimplantation mouse embryos

Nature volume 274, pages 503504 (03 August 1978) | Download Citation

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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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Author information

Affiliations

  1. Departments of Genetics and Medicine, University of Washington, Seattle, Washington 98195

    • PAUL G. KRATZER
    •  & STANLEY M. GARTLER

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DOI

https://doi.org/10.1038/274503a0

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