E-GEOD-46430 - Epe1 recruits the BET family bromodomain protein Bdf2 to establish heterochromatin boundaries

Released on 24 September 2013, last updated on 3 June 2014
Schizosaccharomyces pombe
Samples (4)
Array (1)
Protocols (7)
Heterochromatin spreading leads to the silencing of genes within its path, and boundary elements have evolved to constrain such spreading. In fission yeast, heterochromatin at centromeres I and III is flanked by inverted repeats termed IRCs, which are required for proper boundary functions. However, the mechanisms by which IRCs prevent heterochromatin spreading are unknown. Here, we identified Bdf2, homologous to the mammalian BET family of double bromodomain proteins involved in diverse types of cancers, as a factor required for proper boundary function at IRCs. Bdf2 is enriched at IRCs through its interaction with the boundary protein Epe1. The bromodomains of Bdf2 recognize acetylated histone H4 tails and antagonize Sir2-mediated deacetylation of histone H4K16 to prevent heterochromatin spreading. Our results thus illustrate a mechanism of establishing chromosome boundaries at specific sites through the recruitment of a factor that protects euchromatic histone modifications. They also reveal a previously unappreciated function of H4K16 acetylation, which cooperates with H3K9 methylation to regulate heterochromatin spreading. Two samples, H4K16ac & Bdf2-Flag
Experiment type
ChIP-chip by tiling array 
Investigation descriptionE-GEOD-46430.idf.txt
Sample and data relationshipE-GEOD-46430.sdrf.txt
Raw data (1)E-GEOD-46430.raw.1.zip
Processed data (1)E-GEOD-46430.processed.1.zip
Array designA-GEOD-17079.adf.txt