Journal
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
Volume 368, Issue 1609, Pages -Publisher
ROYAL SOC
DOI: 10.1098/rstb.2011.0336
Keywords
genomic imprinting; DNA methylation; histone modifications; germ cells; epigenomics
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Funding
- l'Agence Nationale de la Recherche (ANR)
- Institut National Contre le Cancer (INCa)
- Ligue National Contre le Cancer
- Agency for International Cancer Research (AICR)
- UK Biotechnology and Biological Sciences Research Council (BBSRC)
- Medical Research Council (MRC)
- BBSRC [BBS/E/B/0000M233] Funding Source: UKRI
- MRC [MR/K011332/1, G0800013] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000M233] Funding Source: researchfish
- Medical Research Council [G0800013, MR/K011332/1] Funding Source: researchfish
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Fundamental to genomic imprinting in mammals is the acquisition of epigenetic marks that differ in male and female gametes at 'imprinting control regions' (ICRs). These marks mediate the allelic expression of imprinted genes in the offspring. Much has been learnt about the nature of imprint marks, the times during gametogenesis at which they are laid down and some of the factors responsible especially for DNA methylation. Recent work has revealed that transcription and histone modifications are critically involved in DNA methylation acquisition, and these findings allow us to propose rational models for methylation establishment. A completely novel perspective on gametic DNA methylation has emerged from epigenomic profiling. Far more differentially methylated loci have been identified in gametes than known imprinted genes, which leads us to revise the notion that methylation of ICRs is a specifically targeted process. Instead, it seems to obey default processes in germ cells, giving rise to distinct patterns of DNA methylation in sperm and oocytes. This new insight, together with the identification of proteins that preserve DNA methylation after fertilization, emphasizes the key role played by mechanisms that selectively retain differential methylation at imprinted loci during early development. Addressing these mechanisms will be essential to understanding the specificity and evolution of genomic imprinting.
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