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Imprinting defects in mouse embryos: stochastic errors or polymorphic phenotype?

S Croteau1, C Polychronakos, A K Naumova

  • 1Department of Obstetrics and Gynecology, Royal Victoria Hospital, Montreal, Canada.

Genesis (New York, N.Y. : 2000)
|October 23, 2001
PubMed
Summary
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Spontaneous imprinting defects, such as loss of H19 imprinting (LOI), occur in mouse embryos. These defects may arise randomly or due to genetic factors, potentially contributing to developmental issues and cancer.

Area of Science:

  • Developmental Biology
  • Genetics
  • Epigenetics

Background:

  • Imprinted genes regulate growth and development; defects are linked to abnormalities and cancer.
  • Understanding spontaneous imprinting defects is crucial for developmental and disease research.

Purpose of the Study:

  • To investigate the occurrence of spontaneous imprinting defects in early mouse embryos.
  • To analyze the expression patterns of imprinted genes H19 and Igf2.

Main Methods:

  • Studied gene expression in individual postimplantation mouse embryos at 7.5 and 8.5 days post-coitum (d.p.c.).
  • Assessed imprinting status by examining the expression of H19 and Igf2.

Main Results:

  • Biallelic expression of H19 (loss of imprinting) was observed in 1.6% of embryos.

Related Experiment Videos

  • Biallelic expression of Igf2 was found in 0.5% of embryos.
  • H19 loss of imprinting (LOI) frequency exceeded human sporadic imprinting disorder incidence.

    • Conclusions:

    • Spontaneous imprinting defects can occur in early mouse embryos, possibly due to stochastic events or genetic factors.
    • These findings suggest mechanisms for polymorphic imprinting and sporadic imprinting defects, including cancer.
    • Discrepancies with human incidence may involve varying error rates, species differences, or prenatal lethality of affected embryos.