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Targeting chromatin machines to promoters in leukemias R. Villa, L. Morey, M. Buschbeck, A. Gutierrez, and L. Di Croce ICREA and Center for Genomic Regulation (CRG), Barcelona, Spain Many human cancers are characterized by alterations in the balance of DNA methylation. In cancer cells, a large part of the genome undergoes dramatic hypomethylation, which is often linked to genome instability, concomitantly with regional gain of methylated sequences at sites usually unmethylated (CpG islands). The major outcome of promoter hypermethylation appears to be long-term silencing of the associated gene. Silencing of tumor suppressors due to such a mechanism can provide a growth advantage to cancer cells. The ability of the PML-RARa fusion protein to block hematopoietic differentiation and to induce acute promyelocytic leukemia is based on aberrant gene repression. Mechanistically, PML-RARa inactivates its target genes by recruiting histone deacetylase (HDAC) and DNA methyltransferase activities to the promoters. We will show that MBD1, a member of a conserved family of proteins able to bind methylated DNA, cooperates with PML-RARa in transcriptional repression and cellular transformation. PML-RARa recruits MBD1 to its target promoter through an HDAC3mediated mechanism. Binding of HDAC3 and MBD1 is not confined to the promoter region but instead is spread over the locus. Retroviral expression of dominant negative mutants of MBD1 in hematopoietic precursors compromised the ability of PML-RARa to block their differentiation and thus restored cell differentiation. Our results demonstrate that PML-RARa functions by recruiting an HDAC3-MBD1 complex that contributes to the establishment and maintenance of the silenced chromatin state. Our results identify MBD1 as a critical mediator of PML-RARa-induced gene silencing subsequent to promoter hypermethylation. Further characterization of the PML-RARa!co-repressor complex, which establishes and allows spreading of the silenced state via Polycomb complex, will be additionally discussed, together with the implication of crosstalk among the different epigenetic layers to the molecular pathology of leukemia. - 40 -
Title to be announced Caroline Dive Cellular and Molecular Pharmacology Group, Paterson Institute for Cancer Research, Christie Hospital NHS Trust, Manchester, United Kingdom (no abstract provided) - 41 -
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Page 5 and 6: Preface In 1998, we organized the f
Page 7 and 8: Acknowledgments This meeting has be
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Page 19 and 20: Regulation of inflammation and gluc
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Epigenetic Regulation of Stem Cell
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Epigenic control of MHC2TA transcri
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Attenuation of MSK1-driven NF-kB ge
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Ubiquitin ligase Smurf1 controls os
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Ambion MicroRNAs (miRNAs) are small
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Organizer: BIOBASE GmbH Date: Janua
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Reliable and efficient gene Knock-d
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Exploring ubiquitin signaling with
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Dr. Nassera Aouali L-1526 Luxembour
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