Enhancer Competition between H19 and Igf2 Does Not Mediate Their Imprinting

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 96; no. 17; pp. 9733 - 9738
• Main Authors: Schmidt, Jennifer V., Levorse, John M., Tilghman, Shirley M.
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences of the United States of America 17.08.1999; National Acad Sciences; National Academy of Sciences; The National Academy of Sciences
• Subjects: Alleles; Animals; Biological Sciences; Chromosomes; DNA; DNA Methylation; Enhancer Elements, Genetic; Epigenetics; Genes; Genes, Tumor Suppressor; Genetic Linkage; Genetic loci; Genetics; Genomic Imprinting; Heterozygote; Insulin-Like Growth Factor II - genetics; Liver; Methylation; Mice; Muscle Proteins - genetics; Promoter Regions, Genetic; RNA; RNA, Long Noncoding; RNA, Untranslated; Rodents; Skeletal muscle
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.96.17.9733

The linked H19 and Igf2 genes on mouse distal chromosome 7 are subject to genomic imprinting. Competition between the promoters of the genes for transcription from shared enhancers has been proposed as an explanation for the coordinate expression and reciprocal imprinting of these two genes. To test this model, we have used Cre-loxP technology to generate in mice a conditional deletion of the H19 promoter and structural gene that leaves no transcription unit in the locus. Contrary to the prediction of enhancer competition we find that transcriptional activity from the H19 promoter is not required for the imprinted silencing of the Igf2 gene.