Schizosaccharomyces pombe
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ABSTRACT:
PROVIDER: PRJNA200317 | ENA |
REPOSITORIES: ENA
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Project description: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
2013-09-24 | E-GEOD-46430 | biostudies-arrayexpress
Project description: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.
2013-09-24 | GSE46430 | GEO
Project description:Loss of Epe1 enhances ectopic heterochromatin formation
| PRJDB6425 | ENA
Project description:Stress can spur the redistribution of histone modifications to establish novel phenotypes. We do not understand how cells leverage existing epigenetic pathways to establish and maintain new gene expression states that enhance fitness and cell survival. H3K9 methylation promotes epigenetic silencing in fission yeast (S. pombe). Heterochromatin establishment depends on the H3K9 methyltransferase, Clr4 and is opposed by two major two heterochromatin regulators, Epe1, a putative H3K9 demethylase and Mst2, an H3K14 acetyltransferase. We designed an inducible system in mst2D cells to toggle Epe1 availability on-demand and trigger heterochromatin misregulation thus initiating an adaptive epigenetic response. Following Epe1 depletion, we mapped transcriptome and H3K9me3 changes as a function of time. Although Epe1 could be removed in ~30 minutes, the population of cells took two orders of magnitude longer to establish an adaptive phenotype. Similarly, re-expressing Epe1 did not switch cells back to their initial state. Instead, cells exhibit unique transcriptional signatures during recovery that encode adaptive memory that is both reversible and tunable. Our results reveal that the slow kinetics of chromatin state changes enable bet-hedging for cells to identify optimal adaptive solutions while hysteresis within the gene regulatory network encodes cellular memory.
2023-07-11 | GSE235807 | GEO
Project description:Stress can spur the redistribution of histone modifications to establish novel phenotypes. We do not understand how cells leverage existing epigenetic pathways to establish and maintain new gene expression states that enhance fitness and cell survival. H3K9 methylation promotes epigenetic silencing in fission yeast (S. pombe). Heterochromatin establishment depends on the H3K9 methyltransferase, Clr4 and is opposed by two major two heterochromatin regulators, Epe1, a putative H3K9 demethylase and Mst2, an H3K14 acetyltransferase. We designed an inducible system in mst2D cells to toggle Epe1 availability on-demand and trigger heterochromatin misregulation thus initiating an adaptive epigenetic response. Following Epe1 depletion, we mapped transcriptome and H3K9me3 changes as a function of time. Although Epe1 could be removed in ~30 minutes, the population of cells took two orders of magnitude longer to establish an adaptive phenotype. Similarly, re-expressing Epe1 did not switch cells back to their initial state. Instead, cells exhibit unique transcriptional signatures during recovery that encode adaptive memory that is both reversible and tunable. Our results reveal that the slow kinetics of chromatin state changes enable bet-hedging for cells to identify optimal adaptive solutions while hysteresis within the gene regulatory network encodes cellular memory.
2023-07-11 | GSE235806 | GEO
Project description:Loss of Epe1 induces epigenetic diversification among epiclones
| PRJDB6424 | ENA
Project description:ChIP-on-chip analyses of JmjC protein Epe1 in fission yeast
| PRJNA95763 | ENA
Project description:CAGE-seq to identify effects of Epe1 OP on transcription start sites in fission yeast.
| PRJDB7027 | ENA
Project description:Bromodomain and Extra-terminal motif (BET) proteins play a central role in transcription regulation and chromatin signalling pathways. In yeast, Bdf1 and its homologous protein Bdf2 are partially redundant and the deletion of both genes is lethal. Most of Bdf1 functions have been investigated in vegetative cells even if this protein is essential for sporulation. In this study, we explored for the first time the functional role of the Bdf1 bromodomains during the sporulation program. Extensive purification of Bdf1 partners identified two independent complexes with Bdf2 or the Swr1 complex. However, none of them are required for meiotic gene regulation or to complete sporulation. Taken together, our results unveil a new role for Bdf1 as a meiotic-specific gene transcriptional regulator independently of its predominant protein partners.
2017-01-11 | PXD005227 | Pride
Project description:Epigenetic adaptation to uncontrolled heterochromatin spreading
| PRJNA258461 | ENA