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DNA methylation variation in cloned mice.
1Cellular Biochemistry, Animal Resource Sciences/Veterinary Medical Sciences, The University of Tokyo, Tokyo, Japan.
Genesis (New York, N.Y. : 2000)
|June 21, 2001
Summary
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.