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Cross-talk between imprinted loci in Prader-Willi syndrome

Nature Genetics volume 46, pages 528530 (2014) | Download Citation

  • A Corrigendum to this article was published on 26 June 2014

This article has been updated

Prader-Willi syndrome (PWS) is caused by loss of paternally expressed genes at an imprinted locus on chromosome 15, including the long noncoding RNA IPW. A new study identifies a critical role for IPW in modulating the expression of maternally expressed genes in trans, which has important implications for the understanding of imprinted gene networks.

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Change history

  • 13 June 2014

    In the version of this article initially published, the following sentence on page 529 referred to an incorrect locus (in bold): "In mice, the lncRNA Kcnq1ot1 associates with G9a and the polycomb repressive complex 2 (PRC2) to regulate the expression of other genes in the Dlk1-Dio3 locus in cis." The correct locus is Kcnq1. The error has been corrected in the HTML and PDF versions of the article.

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Author information

Affiliations

  1. Adele Murrell is in the Department of Biology and Biochemistry, Centre for Regenerative Medicine, University of Bath, Bath, UK.

    • Adele Murrell

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Competing interests

The author declares no competing financial interests.

Corresponding author

Correspondence to Adele Murrell.

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DOI

https://doi.org/10.1038/ng.2994

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