Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Brief Communication
  • Published:

The callipyge mutation enhances the expression of coregulated imprinted genes in cis without affecting their imprinting status

Abstract

The callipyge (CLPG) phenotype (from καλι, “beautiful,” and πιγɛ, “buttocks”) described in sheep is an inherited muscular hypertrophy that is subject to an unusual parent-of-origin effect referred to as polar overdominance: only heterozygous individuals having inherited the CLPG mutation from their sire exhibit the muscular hypertrophy1. The callipyge (clpg) locus was mapped to a chromosome segment of approximately 400 kb (refs. 24), which was shown to contain four genes (DLK1, GTL2, PEG11 and MEG8) that are preferentially expressed in skeletal muscle and subject to parental imprinting in this tissue5,6,7,8,9. Here we describe the effect of the CLPG mutation on the expression of these four genes, and demonstrate that callipyge individuals have a unique expression profile that may account for the observed polar overdominance.

This is a preview of subscription content, access via your institution

Access options

Buy this article

Prices may be subject to local taxes which are calculated during checkout

Figure 1: Evaluation of the transcript levels and imprinting status of DLK1, PEG11, GTL2 and MEG8 in skeletal muscle (longissimus dorsi) of eight-week individuals representing the four possible callipyge genotypes: wild type, CLPGM/+P, +M/CLPGP and CLPG/CLPG.
Figure 2: A model for the callipyge polar overdominance.

Similar content being viewed by others

References

  1. Cockett, N.E. et al. Science 273, 236–238 (1996).

    Article  CAS  Google Scholar 

  2. Shay, T. et al. Mamm. Genome 12, 141–149 (2001).

    Article  CAS  Google Scholar 

  3. Segers, K. et al. Anim. Genet. 31, 352–359 (2001).

    Article  Google Scholar 

  4. Berghmans, S. et al. Mamm. Genome 12, 183–185 (2001).

    Article  CAS  Google Scholar 

  5. Charlier, C. et al. Genome Res. (in press).

  6. Miyoshi, N. et al. Genes Cells 5, 211–220 (2000).

    Article  CAS  Google Scholar 

  7. Schmidt, J.V. et al. Genes Dev. 14, 1997–2002 (2000).

    CAS  PubMed  PubMed Central  Google Scholar 

  8. Takada, S. et al. Curr. Biol. 10, 1135–1138 (2000).

    Article  CAS  Google Scholar 

  9. Wylie, A.A. et al. Genome Res. 10, 1711–1718 (2000).

    Article  CAS  Google Scholar 

Download references

Acknowledgements

We thank A. Ferguson-Smith and M. Paulsen for discussions. This project was supported by grants from Fonds de la Recherche Fondamentale Collective (n° 2.4525.96), Crédit aux Chercheurs (n° 1.5.134.00) from the Fonds National de la Recherche Scientifique, Crédit à la Recherche from the University of Liège, the Utah Center of Excellence Program, the USDA/NRI Competitive Grants Program (USDA/NRICGP grants 94-04358, 96-35205 and 98-03455) and the Utah Agricultural Experiment Station.

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Michel Georges.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Charlier, C., Segers, K., Karim, L. et al. The callipyge mutation enhances the expression of coregulated imprinted genes in cis without affecting their imprinting status. Nat Genet 27, 367–369 (2001). https://doi.org/10.1038/86856

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1038/86856

This article is cited by

Search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing