International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)


I24. Expression of Imprinted Genes in Mice Deficient for PcG Proteins

Naomi Tsujimoto1, Haruhiko Koseki2, Yoshihiro Takihara3, Yuko Katoh-Fukui4 and Hiroyuki Sasaki1
1Division of Human Genetics, Department of Integrated Genetics, National Institute of Genetics, Yata, Mishima, Shizuoka 411-8540; 2Division of Molecular Immunology, Center for Biomedical Science, School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-0856; 3Depertment of Medical Genetics, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamadaoka, Suita, Osaka 585; 4Mitsubishi Kasei Institute of Life Science, Machida, Tokyo 194-8511, Japan.

The paternal and maternal genomes of mammals are not equivalent in their function and both are required for normal development. This functional non-equivalence is due to gamete-specific differential modifications conferred by a process known as genomic imprinting. Since the Polycomb group (PcG) proteins form multimeric, chromatin-associated complexes involved in stable and heritable repression of gene activity, they might be involved in the process of genomic imprinting. To investigate this possibility, we analyzed the allelic expression patterns of five imprinted genes, H19, Igf2, Peg3, Peg5 and Snrpn, in mouse embryos deficient for two PcG proteins, mel-18 and bmi-1. All of the imprinted genes were expressed in the normal allele-specific fashions, suggesting that the products of mel-18 and bmi-1 are not required for the imprinted expression of these genes. We also studied the expression levels of H19 and Igf2 in embryos deficient for M33 or Rae28, which also belong to the PcG proteins. Again, either mutation did not affect the expression levels of H19 and Igf2. We conclude that these four PcG proteins are not directly involved in the imprinted expression of these genes.


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