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

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


  • 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



Publication Data

November 2, 2001

Associated Grants


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