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Journal of Cell Science, Vol 112, Issue 24 4627-4639, Copyright © 1999 by Company of Biologists
JOURNAL ARTICLES |
JW Voncken, D Schweizer, L Aagaard, L Sattler, MF Jantsch and M van Lohuizen
The Netherlands Cancer Institute, Division of Molecular Carcinogenesis, NL-1066 CX Amsterdam, The Netherlands.
The human proto-oncogene Bmi1 is a member of the mammalian Polycomb Group (Pc-G) genes. The subnuclear distribution of the BMI1 protein was studied in several primary human and tumor-derived cell lines using immunohistochemical and biochemical methods. In primary and tumor cells, nuclear BMI1 shows a fine-grain distribution over chromatin, usually dense in interphase nuclei and significantly weaker along mitotic chromosomes. In addition, BMI1 preferentially associates with several distinct heterochromatic domains in tumor cell lines. In both primary and tumor cell lines a marked cell cycle-regulation of Pc-G-chromatin interaction is observed: nuclear BMI1-staining dissipates in late S phase and is re-established early in G(1)-phase. Chromatin-association of BMI1 inversely correlates with its phosphorylation status in a cell cycle-dependent fashion: at G(1)/S, hypophosphorylated BMI1 is specifically retained in the chromatin-associated nuclear protein fraction, whereas during G(2)/M, phosphorylated BMI1 is not chromatin-bound. Our findings indicate a strict cell cycle-controlled regulation of Pc-G complex-chromatin association and provide molecular tools for improving our understanding of Pc-G complex regulation and function in mammalian cells.
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