Journal
G3-GENES GENOMES GENETICS
Volume 3, Issue 10, Pages 1785-1794Publisher
GENETICS SOC AM
DOI: 10.1534/g3.113.007534
Keywords
Chromator; Nipped-B; Putzig; RNA polymerase; Suppressor of Hairless
Categories
Funding
- National Institutes of Health [R01GM055683, P01 HD052860]
- Saint Louis University Presidential Fellowship
Ask authors/readers for more resources
The cohesin protein complex functionally interacts with Polycomb group (PcG) silencing proteins to control expression of several key developmental genes, such as the Drosophila Enhancer of split gene complex [E(spl)-C]. The E(spl)-C contains 12 genes that inhibit neural development. In a cell line derived from the central nervous system, cohesin and the PRC1 PcG protein complex bind and repress E (spl)-C transcription, but the repression mechanisms are unknown. The genes in the E(spl)-C are directly activated by the Notch receptor. Here we show that depletion of cohesin or PRC1 increases binding of the Notch intracellular fragment to genes in the E(spl)-C, correlating with increased transcription. The increased transcription likely reflects both direct effects of cohesin and PRC1 on RNA polymerase activity at the E(spl)-C, and increased expression of Notch ligands. By chromosome conformation capture we find that the E(spl)-C is organized into a self-interactive architectural domain that is co-extensive with the region that binds cohesin and PcG complexes. The self-interactive architecture is formed independently of cohesin or PcG proteins. We posit that the E(spl)-C architecture dictates where cohesin and PcG complexes bind and act when they are recruited by as yet unidentified factors, thereby controlling the E(spl)-C as a coordinated domain.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available