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Genomic imprinting

Making sense or antisense?

Nature volume 389, pages 669–671 (1997)Cite this article

Genomic imprinting is a genetic mechanism by which genes are expressed from the maternal or paternal chromosomes1, and loss of imprinting is involved in a variety of diseases and cancers. All the imprinted genes that have been studied so far have regions in which the maternal and paternal DNA copies are methylated differently at CpG residues — cytosine-guanine base pairs. So DNA methylation is suspected to be the signal from the parental germ cells that results in the allele-specific expression of imprinted genes. Indeed, in mice that do not have methylation (because of mutation in the methyltransferase gene), imprinting is altered2.

The exciting work reported by Wutz et al3 on page745 of this issue now shows that differentially methylated regions in a specific imprinted gene ( Igf2r ; the maternally expressed gene that encodes the type-2 receptor for insulin-like growth factor) can carry a crucial imprinting signal. When this region is deleted from Igf2r, the gene loses its imprinting and is expressed regardless of parental origin. Moreover, the authors show that the deleted region (which is in an intron of Igf2r ) is normally the promoter of an antisense transcript that is expressed from the paternal chromosome. Intriguingly, when the antisense gene is expressed, the sense is not, and vice versa, indicating that some form of ‘expression competition’ regulates imprinting of Igf2r, as it apparently also does with other imprinted loci4,5.

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Figure 1: Wutz et al.3 have shown that differentially methylated regions in the Igf2r gene can carry a critical imprinting signal.
Figure 2: Models for paternal silencing of Igf2r.

References

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Authors and Affiliations

  1. the Laboratory of Developmental Genetics and Imprinting, The Babraham Institute, Cambridge, CB2 4AT, UK

    Wolf Reik & Miguel Constancia

Authors
  1. Wolf Reik
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  2. Miguel Constancia
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Reik, W., Constancia, M. Making sense or antisense?. Nature 389, 669–671 (1997). https://doi.org/10.1038/39461

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