International Mammalian Genome Society

logo18th International Mouse Genome Conference

17-22 October 2004, Seattle, USA


POSTER 39 - THE REQUIREMENT FOR EED IN AUTOSOMAL GENOMIC IMPRINTING MAY BE TISSUE SPECIFIC

Chamberlain SJ, Montgomery ND, Kalantry S, Magnuson T

Department of Genetics, University of North Carolina-Chapel Hill, Chapel Hill, NC, United States

EED and EZH2 –containing Polycomb group (PcG) complexes are dynamic and maintain transcriptionally repressive chromatin states through replication and mitosis. In addition to their role in the maintenance of expression patterns of homeotic genes, these complexes also act upon other genes to maintain cellular differentiation in such processes as development, hematopoiesis, and tumorigenesis.

Mice with mutations in the Eed gene display defects in imprinted X-inactivation and autosomal imprinting.  The major defect is a failure to maintain transcriptional repression in the silenced chromosome or alleles. Data from this lab suggests that the failure to maintain silencing on the inactive X-chromosome occurs only in tissues that undergo imprinted X-inactivation, and that it is most pronounced in differentiating cells of the trophoblast, while the primitive endoderm and the undifferentiated trophoblast cells appear to correctly maintain the inactive X in the absence of EED.  Here we utilize a gene-trap reporter construct, and a conventional targeted mutation to determine whether the defects in autosomal imprinting in Eed mutants are similarly restricted to a particular tissue type or suggestive of a particular differentiation state in mouse embryos.

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