DNA methylation, chromatin boundaries, and mechanisms of genomic imprinting.
In mammals, the maternal and paternal genomes are both required for normal embryonic and postnatal development. As a consequence, the majority of genes possess a bi-allelic pattern of expression, with the exception of certain loci where transcription is strictly dependent on parental origin. This alternative, termed genomic imprinting, is an epigenetic form of gene regulation that allows controlled expression of one parental allele. Experimental evidence supports the idea that chromatin organization, DNA methylation, replication timing, genomic domain organization, and more recently methylation-dependent boundary function are key components of imprinting mechanisms. Imprinted genes are mainly required during embryogenesis and development, but loss of controlled imprinting has direct consequences in carcinogenesis. For example, imprinted tumor suppressor genes and proto-oncogenes are highly susceptible to allelic inactivation or in contrast to activation that induces tumorigenic processes. Therefore, genomic imprinting represents one of the more challenging and interesting scientific and medical topics, and especially because a large combinatorial set of possibilities for gene regulation arises from the increasing number of imprinted loci identified.
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Departamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México (UNAM), Mexico City, Mexico. luisbenbri@mexis.com
D000483:Alleles; D000818:Animals; D002843:Chromatin / Q000648:ultrastructure*; D019175:DNA Methylation; D005786:Gene Expression Regulation; D018392:Genomic Imprinting; D006801:Humans; D007335:Insulin-Like Growth Factor II / Q000235:genetics; D008954:Models, Biological; D008957:Models, Genetic; D017434:Protein Structure, Tertiary; D062085:RNA, Long Noncoding; D022661:RNA, Untranslated / Q000235:genetics
D002843:Chromatin; C094335:H19 long non-coding RNA; D062085:RNA, Long Noncoding; D022661:RNA, Untranslated; D007335:Insulin-Like Growth Factor II