Parental Imprinting of the H19 and Igf2 Genes in the Mouse

  1. S.M. Tilghman,
  2. M.S. Bartolomei*,
  3. A.L. Webber,
  4. M.E. Brunkow,
  5. J. Saam,
  6. P.A. Leighton,
  7. K. Pfeifer, and
  8. S. Zemel
  1. Howard Hughes Medical Institute and Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544

This extract was created in the absence of an abstract.

Excerpt

A long-standing assumption of Mendelian genetics was that autosomal genes, present in two copies in diploid organisms, were functionally equivalent. The discovery of the phenomenon of parental or genomic imprinting has now firmly established that this is not always the case in mammals. The functional non-equivalence of the maternal and paternal genomes was first suspected because of the failure to observe parthenogenesis in mammals. This was confirmed with the elegant nuclear transplantation studies pioneered by McGrath and Solter (1983, 1984). Although these experiments, and others that followed in their wake (Surani et al. 1984, 1986; McGrath and Solter 1986), established the requirement for both parental pronuclei and led directly to the notion of genes inherited in differentially active states, they could not make any predictions about the number of such genes.

Using classic genetics, B. Cattanach, A.G. Searle, and C.V. Beechey have over the years generated an “imprinting map” of...

  • *

    * Present address: Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104

  • Present address: Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5 Canada.

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