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

TitleLoss of the Suv39h histone methyltransferases impairs mammalian heterochromatin and genome stability.
Publication TypeJournal Article
Year of Publication2001
AuthorsPeters AH, O'Carroll D, Scherthan H, Mechtler K, Sauer S, Schöfer C, Weipoltshammer K, Pagani M, Lachner M, Kohlmaier A, Opravil S, Doyle M, Sibilia M, Jenuwein T
JournalCell
Volume107
Issue3
Pagination323-37
Date Published2001 Nov 2
ISSN0092-8674
KeywordsAneuploidy, 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
Abstract

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.

Alternate JournalCell
PubMed ID11701123
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