Uncoupling of Genomic and Epigenetic Signals in the Maintenance and Inheritance of Heterochromatin Domains in Fission Yeast
| Autor: | Kristin C. Scott, Huntington F. Willard, Bayly S. Wheeler, Brandon T. Ruderman |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Transcription
Genetic Heterochromatin Gene Expression Genomics Biology Investigations Models Biological Epigenesis Genetic Chromosome segregation Gene Expression Regulation Fungal Gene Order Schizosaccharomyces Genetics Constitutive heterochromatin Epigenetics Gene Silencing Enhancer Chromatin Meiosis Genetic Loci Heterochromatin protein 1 Genome Fungal Cell Division |
| Zdroj: | Genetics |
| ISSN: | 1943-2631 0016-6731 |
| Popis: | Many essential aspects of genome function, including gene expression and chromosome segregation, are mediated throughout development and differentiation by changes in the chromatin state. Along with genomic signals encoded in the DNA, epigenetic processes regulate heritable gene expression patterns. Genomic signals such as enhancers, silencers, and repetitive DNA, while required for the establishment of alternative chromatin states, have an unclear role in epigenetic processes that underlie the persistence of chromatin states throughout development. Here, we demonstrate in fission yeast that the maintenance and inheritance of ectopic heterochromatin domains are independent of the genomic sequences necessary for their de novo establishment. We find that both structural heterochromatin and gene silencing can be stably maintained over an ∼10-kb domain for up to hundreds of cell divisions in the absence of genomic sequences required for heterochromatin establishment, demonstrating the long-term persistence and stability of this chromatin state. The de novo heterochromatin, despite the absence of nucleation sequences, is also stably inherited through meiosis. Together, these studies provide evidence for chromatin-dependent, epigenetic control of gene silencing that is heritable, stable, and self-sustaining, even in the absence of the originating genomic signals. |
| Databáze: | OpenAIRE |
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