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Loss of the Suv39h histone methyltransferases impairs mammalian heterochromatin and genome stability.

Cell | Nov 2, 2001

Histone H3 lysine 9 methylation has been proposed to provide a major "switch" for the functional organization of chromosomal subdomains. Here, we show that the murine Suv39h histone methyltransferases (HMTases) govern H3-K9 methylation at pericentric heterochromatin and induce a specialized histone methylation pattern that differs from the broad H3-K9 methylation present at other chromosomal regions. Suv39h-deficient mice display severely impaired viability and chromosomal instabilities that are associated with an increased tumor risk and perturbed chromosome interactions during male meiosis. These in vivo data assign a crucial role for pericentric H3-K9 methylation in protecting genome stability, and define the Suv39h HMTases as important epigenetic regulators for mammalian development.

Pubmed ID: 11701123 RIS Download

Mesh terms: Aneuploidy | Animals | Chromosome Segregation | Fibroblasts | Gene Targeting | Genome | Germ Cells | Heterochromatin | Histone-Lysine N-Methyltransferase | Histones | Hypogonadism | Lymphoma, B-Cell | Male | Mammals | Meiosis | Methylation | Methyltransferases | Mice | Mice, Knockout | Mice, Mutant Strains | Mutagenesis | Protein Methyltransferases | Repressor Proteins | Sex Chromosome Aberrations | Spermatocytes | Spermatogenesis

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Mouse Genome Informatics (Data, Gene Annotation)

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