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First published online 12 January 2005
doi: 10.1242/dev.01612

Development 132, 635-644 (2005)
Published by The Company of Biologists 2005
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Lsh controls silencing of the imprinted Cdkn1c gene

Tao Fan1, John P. Hagan2, Serguei V. Kozlov2, Colin L. Stewart2 and Kathrin Muegge1,*

1 Laboratory of Molecular Immunoregulation, Basic Research Program, SAIC-Frederick, National Cancer Institute, Frederick, MD 21702-1201, USA
2 Cancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, MD 21702-1201, USA

* Author for correspondence (e-mail: muegge{at}ncifcrf.gov)

Accepted 26 November 2004

Epigenetic regulation, such as DNA methylation plays an important role in the control of imprinting. Lsh, a member of the SNF2 family of chromatin remodeling proteins, controls DNA methylation in mice. To investigate whether Lsh affects imprinting, we examined CpG methylation and allelic expression of individual genes in Lsh-deficient embryos. We report here that loss of Lsh specifically alters expression of the Cdkn1c gene (also known as p57(Kip2)) but does not interfere with maintenance of imprints at the H19, Igf2, Igf2r, Zac1 and Meg9 genes. The reactivation of the silenced paternal Cdkn1c allele correlates closely with a loss of CpG methylation at the 5' DMR at the Cdkn1c promoter, whereas KvDMR1 and DMRs of other imprinted genes were not significantly changed. Chromatin immunoprecipitations demonstrate a direct association of Lsh with the 5' DMR at the Cdkn1c promoter, but not with Kv DMR1 or other imprinted loci. These data suggest that methylation of the 5' DMR plays an important role in the imprinting of the Cdkn1c gene. Furthermore, it suggests that Lsh is not required for maintenance of imprinting marks in general, but is only crucial for imprinting at distinct genomic sites.

Key words: Chromatin structure, DNA methylation, Gene imprinting, Lsh


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