期刊
MOLECULAR CELL
卷 19, 期 5, 页码 707-716出版社
CELL PRESS
DOI: 10.1016/j.molcel.2005.07.022
关键词
-
资金
- Intramural NIH HHS Funding Source: Medline
The silenced HMR domain is restricted from spreading by barrier elements, and the right barrier is a unique t-RNAT(THR) gene. We show that sequences immediately flanking the silenced domain were enriched in acetylated, but not methylated, histones, whereas the barrier element was associated with a nucleosome-free region. Surprisingly, the SAGA acetyltransferase resided across the entire region. We further demonstrate that a mutation in the barrier eliminated the nucleosome-free gap but only subtly altered the distribution of SAGA. Interestingly, neither reformation of the nucleosome nor mutations in chromatin-modifying enzymes alone led to an unrestricted spread of silenced chromatin. Double mutations in the t-RNA barrier and these complexes, on the other hand, led to a significant spread of Sir proteins. These results suggest two overlapping mechanisms function to restrict the spread of silencing: one of which involves a DNA binding element, whereas the other mechanism involves specific chromatin-modifying activities.
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