Chromocentre integrity and epigenetic marks
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
19766725
DOI
10.1016/j.jsb.2009.09.007
PII: S1047-8477(09)00251-2
Knihovny.cz E-resources
- MeSH
- Cell Line MeSH
- Epigenesis, Genetic genetics MeSH
- Heterochromatin metabolism MeSH
- Histone-Lysine N-Methyltransferase genetics physiology MeSH
- Histone Methyltransferases MeSH
- Histones metabolism MeSH
- Methylation MeSH
- Mice MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Heterochromatin MeSH
- Histone-Lysine N-Methyltransferase MeSH
- Histone Methyltransferases MeSH
- Histones MeSH
The epigenetic modification of histones dictates the formation of euchromatin and heterochromatin domains. We studied the effects of a deficiency of histone methyltransferase, SUV39h, and trichostatin A-dependent hyperacetylation on the structural stability of centromeric clusters, called chromocentres. We did not observe the expected disintegration of chromocentres, but both SUV39h deficiency and hyperacetylation in SUV39h+/+ cells induced the re-positioning of chromocentres closer to the nuclear periphery. Conversely, TSA treatment of SUV39h-/- cells re-established normal nuclear radial positioning of chromocentres. This structural re-arrangement was likely caused by several epigenetic events at centromeric heterochromatin. In particular, reciprocal exchanges between H3K9me1, H3K9me2, H3K9me3, DNA methylation, and HP1 protein levels influenced chromocentre nuclear composition. For example, H3K9me1 likely substituted for the function of H3K9me3 in chromocentre nuclear arrangement and compaction. Our results illustrate the important and interchangeable roles of epigenetic marks for chromocentre integrity. Therefore, we propose a model for epigenetic regulation of nuclear stability of centromeric heterochromatin in the mouse genome.
References provided by Crossref.org
H3K9me3 and H4K20me3 represent the epigenetic landscape for 53BP1 binding to DNA lesions
SUV39h-independent association of HP1 beta with fibrillarin-positive nucleolar regions
