• Register
X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

X

Leaving Community

Are you sure you want to leave this community? Leaving the community will revoke any permissions you have been granted in this community.

No
Yes

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

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

Journal

Cell

Publication Data

November 2, 2001

Associated Grants

None

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