Abnormal development of embryonic and extraembryonic cell lineages in parthenogenetic mouse embryos

Authors

  • Karin S. Sturm,

    Corresponding author
    1. Laboratory of Radiobiology and Environmental Health, University of California, San Francisco, California 94143-0750
    Current affiliation:
    1. Children's Medical Research Institute, Locked Bag 23, Wentworthville, NSW 2145, Australia
    • Laboratory of Radiobiology and Environmental Health, University of California, San Francisco, California 94143-0750
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  • Margaret L. Flannery,

    1. Laboratory of Radiobiology and Environmental Health, University of California, San Francisco, California 94143-0750
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  • Roger A. Pedersen

    1. Laboratory of Radiobiology and Environmental Health, University of California, San Francisco, California 94143-0750
    2. Department of Radiology, Anatomy, and Obstetrics, Gynaecology and Reproductive Sciences, University of California, San Francisco, California 94143-0750
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Abstract

Parthenogetically activated, diploid mouse oocytes can develop to midgestation stages in utero. However, even these advanced parthenogenones appear to die because of much reduced trophoblast and yolk sac development. Previous studies have compared the general features of parthenogenetic and androgenetic development and determined the fate of uniparental cells in chimeras with normal embryos. These studies led to the concept of genomic imprinting as the cause for developmental failure when either the maternal or the paternal genome is duplicated, with the corresponding deficiency of the other. Genomic imprinting appears to arise during gametogenesis and to act through dosage effects in a set of imprinted genes, whose expression depends on their parental origin. In this study we undertook a more detailed morphological analysis of parthenogenetic development in the mouse and established a classification system to quantify the developmental extent of parthenogenones. We found that the failure of parthenogenones occurred at different times during early postimplantation development, generating a spectrum of concepti which had developed to different extents, with only a small fraction of the embryos reaching advanced somite stages. In all parthenogenones differentiation and proliferation of the trophectoderm and primitive endoderm lineages (both extraembryonic) was abnormal, and in all, even the best-developed parthenogenones, we observed similar deficiencies in the embryonic lineages, especially the mesoderm. Common to all abnormally developed lineages was that the proportion of undifferentiated precursor cells was much reduced, while their differentiated descendants were relatively abundant. We propose, therefore, that the failure of parthenogenones to develop to term is due to abnormal regulation of differentiation and proliferation in both embryonic and extraembryonic lineages. In this hypothesis, the apparent tissue specific defects observed in parthenogenones arise as a consequence of the functional importance of certain tissues (like the trophoblast) early in development. The spectrum of parthenogenones thus appears to reflect critical events in early development, whose regulation are affected by genomic imprinting. © 1994 Wiley-Liss, Inc.

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