|Title||Loss of the Suv39h histone methyltransferases impairs mammalian heterochromatin and genome stability.|
|Publication Type||Journal Article|
|Year of Publication||2001|
|Authors||Peters 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|
|Date Published||2001 Nov 2|
|Keywords||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|
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.