Imprinted expression of the Igf2r gene depends on an intronic CpG island

Anton Wutz, Oskar W. Smrzka, Norbert Schweifer, Karl Schellander, Erwin F. Wagner and Denise P. Barlow ()
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Anton Wutz: Institute of Molecular Pathology
Oskar W. Smrzka: The Netherlands Cancer Institute (H5)
Norbert Schweifer: Boehringer-Ingelheim R&D
Karl Schellander: Rheinische Friedrich-Wilhelms Universität Bonn
Erwin F. Wagner: Institute of Molecular Pathology
Denise P. Barlow: The Netherlands Cancer Institute (H5)

Nature, 1997, vol. 389, issue 6652, 745-749

Abstract: Abstract Gametic imprinting is a developmental process that induces parental-specific expression or repression of autosomal and X-chromosome-linked genes1,2. The mouse Igf2r gene (encoding the receptor for insulin- like growth factor type-2) is imprinted and is expressed from the maternal allele after embryonic implantation3. We previously proposed that methylation of region 2, a region rich in cytosine-guanine doublets (a ‘CpG island’) in the second intron of Igf2r, is the imprinting signal that maintains expression of the maternal allele4. Here we use mouse transgenes to test the role of region 2 and the influence of chromosome location on Igf2r imprinting. Yeast artificial chromosome transgenes successfully reproduced the imprinted methylation and expression pattern of the endogenous Igf2r gene; deletion of region 2 from these transgenes caused a loss of imprinting and restored biallelic Igf2r expression. These results define a primary role for region 2 and a negligible role for chromosomal location in Igf2r imprinting; they also show that methylation imprints can maintain allelic expression. Short transgenes containing only region 2 and yeast artificial chromosome transgenes with an inactive Igf2r promoter do not attract parental-specific methylation. All transgenes showing paternal-specific repression of Igf2r produced an antisense RNA whose transcription was dependent on region 2. The production of an antisense RNA by the repressed parental allele is reminiscent of the imprinting of the Igf2/H19 gene pair5 and may indicate that expression competition could play a general role in imprinting.

Date: 1997
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DOI: 10.1038/39631

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