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DNA methylation variation in cloned mice

J Ohgane1, T Wakayama, Y Kogo

  • 1Cellular Biochemistry, Animal Resource Sciences/Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan.

Genesis (New York, N.Y. : 2000)
|June 21, 2001
PubMed

Insights

Mammalian cloning via nuclear transfer shows low success rates and abnormal offspring due to incomplete DNA methylation reprogramming. Aberrant methylation in cloned animals primarily affects tissue-specific sites, indicating imperfect genomic copies.

Area of Science:

  • Epigenetics
  • Mammalian Cloning
  • Developmental Biology

Background:

  • Mammalian cloning by nuclear transfer has limitations, including low production rates and developmental abnormalities in offspring.
  • Incomplete epigenetic reprogramming, specifically DNA methylation, is a suspected cause of these cloning inefficiencies.

Purpose of the Study:

  • To investigate DNA methylation patterns in cloned mammals.
  • To identify potential epigenetic causes for low cloning success rates and abnormal phenotypes.

Main Methods:

  • Analysis of tissue-specific DNA methylation patterns in normal B6D2F1 mice (placenta, skin, kidney).
  • Comparison of methylation profiles in cloned fetuses with normal controls.
  • Identification and characterization of aberrantly methylated CpG islands in cloned animals.

Main Results:

  • Seven tissue-specific methylated CpG islands were identified in normal mice.
  • Four CpG islands showed aberrant methylation or were unmethylated in cloned fetuses.
  • Aberrant methylation in clones predominantly occurred at tissue-specific loci, with variations between individual clones.

Conclusions:

  • Incomplete reestablishment of DNA methylation patterns is a significant issue in mammalian cloning.
  • Aberrant methylation, particularly at tissue-specific sites, contributes to developmental abnormalities in cloned animals.
  • Cloned animals exhibit epigenetic variations, meaning they are not exact genetic replicas of the donor.

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