Widespread disruption of genomic imprinting in adult interspecies mouse (Mus) hybrids
Article first published online: 6 SEP 2005
Copyright © 2005 Wiley-Liss, Inc.
Volume 43, Issue 3, pages 100–108, November 2005
How to Cite
Shi, W., Krella, A., Orth, A., Yu, Y. and Fundele, R. (2005), Widespread disruption of genomic imprinting in adult interspecies mouse (Mus) hybrids. Genesis, 43: 100–108. doi: 10.1002/gene.20161
- Issue published online: 8 NOV 2005
- Article first published online: 6 SEP 2005
- Manuscript Accepted: 4 AUG 2005
- Manuscript Received: 5 APR 2005
- Swedish Research Council (Vetenskapsrådet and the Wallenberg Consortium North)
- interspecies hybridization;
- DNA methylation
Mammalian interspecies hybrids exhibit parent-of-origin effects in that offspring of reciprocal matings, even though genetically identical, frequently exhibit opposite phenotypes, especially in growth. This was also observed in hybridization with the genus Mus. These parent-of-origin effects suggested that imbalance in the expression of imprinted genes, which are expressed differentially, depending on their transmission through the maternal or paternal germline, and/or differential loss-of-imprinting (LOI) could underlie these opposite growth phenotypes in reciprocal mammalian hybrids. Here we report that tissue-specific LOI occurs in adult Mus hybrids. Contrary to expectations, LOI patterns were not consistent with a direct influence of altered expression levels of imprinted genes on growth. Bisulfite sequencing revealed that reactivation of maternal alleles of Peg3 and Snrpn in specific tissues was accompanied by partial demethylation at their potential imprinting control regions. We propose that abnormal reprogramming after fertilization and during preimplantation development is in part responsible for hybrid dysgenesis, for which a strong epigenetic basis has been demonstrated. genesis 43:100–108, 2005. © 2005 Wiley-Liss, Inc.