Mapping the dynamics of epigenetic adaptation during heterochromatin misregulation [ChIP-seq]
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ABSTRACT:
PROVIDER: PRJNA987655 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25024322_1.fastq.gz | Fastqsanger.gz | |||
| SRR25024322_2.fastq.gz | Fastqsanger.gz | |||
| SRR25024323_1.fastq.gz | Fastqsanger.gz | |||
| SRR25024323_2.fastq.gz | Fastqsanger.gz | |||
| SRR25024324_1.fastq.gz | Fastqsanger.gz |
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Project description:Mapping the dynamics of epigenetic adaptation during heterochromatin misregulation
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Project description:Mapping the dynamics of epigenetic adaptation during heterochromatin misregulation [RNA-seq]
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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: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:This SuperSeries is composed of the SubSeries listed below.
2023-07-11 | GSE235808 | GEO
Project description:Heterochromatin, a highly compact chromatin state characterized by histone H3 lysine 9 methylation (H3K9me) and HP1 protein binding, epigenetically silences the underlying DNA and influences the expression of neighboring genes. Therefore the sites of heterochromatin assembly and its subsequent spreading are generally precisely determined. Here we show that in fission yeast, the combined absence of anti-silencing factors Mst2 and Epe1 results in uncontrolled heterochromatin spreading and severe growth defects. Interestingly, these cells quickly recover by accumulating H3K9me at the clr4+ locus, which encodes the H3K9 methyltransferase essential for heterochromatin assembly, thereby leading to reduced expression of Clr4 to restrain heterochromatin spreading. Preventing H3K9me at the clr4+ locus resulted in the accumulation of H3K9me at the rik1+ locus, which encodes another component of the Clr4 complex essential for H3K9me. Our results demonstrate that promiscuous heterochromatin assembly enables fast adaptation in response to changes in chromatin landscape and illustrate a negative feedback mechanism by which cells counteract toxic heterochromatin accumulation.
2015-03-13 | GSE60521 | GEO
Project description:Heterochromatin, a highly compact chromatin state characterized by histone H3K9 methylation and HP1 protein binding, silences the underlying DNA and influences the expression of neighboring genes. However, the mechanisms that regulate heterochromatin spreading are not well understood. In this study, we show that the conserved Mst2 histone acetyltransferase complex in fission yeast regulates histone turnover at heterochromatin regions to control heterochromatin spreading and prevents ectopic heterochromatin assembly. The combined loss of Mst2 and the JmjC domain protein Epe1 results in uncontrolled heterochromatin spreading and massive ectopic heterochromatin, leading to severe growth defects due to the inactivation of essential genes. Interestingly, these cells quickly recover by accumulating heterochromatin at genes essential for heterochromatin assembly, leading to their reduced expression to restrain heterochromatin spreading. Our studies discover redundant pathways that control heterochromatin spreading and prevent ectopic heterochromatin assembly and reveal a fast epigenetic adaptation response to changes in heterochromatin landscape.
| S-EPMC4395908 | biostudies-literature
Project description:Adaptation dynamics in stressful environments from standing genetic variation in S. cerevisiae
| PRJEB46680 | ENA
Project description:How heterochromatin genes evolve as ‘gene islands’ to fit into the repressive chromatin environment in plants are poorly understood. To address this question, we performed a comprehensive epigenetic profiling in the genus Oryza with high quality BAC-assembled regional sequences and near gap-free genomes. Comparative analyses of a heterochromatin knob demonstrated the dynamics of chromatin states (heterochromatin versus euchromatin) among the Oryza species in a phylogenetic context. LTR (long-terminal repeat) retrotransposons are the main contributor (~99%) to heterochromatin diversity. Heterochromatin genes are distributed as ‘gene islands’ in heterochromatin, but heterochromatin hardly projects expression disturbance to them. Heterochromatin genes are almost free of H3K9me2 histone modifications in exons, and have similar gene structure and transposon invasion rate in introns to its orthologous euchromatin counterparts. Analyses of the rice HiC data verified the topological existence of ‘gene islands’ and demonstrated that ‘gene islands’ are less spatially co-localized with heterochromatin. By examining evolutionarily recent inserted genes in the Oryza species, we found that the active promoters of six inserted genes can elevate CHH (H=A, C, T) methylation at the insertion sites. Our results reveals that heterochromatin genes evolve as heterochromatin-insulated ‘gene islands’ to escape the repressive influence of heterochromatin, contrasting to the ‘integration’ model in Drosophila. We suggest that active gene promoters may contribute to this insulation by acting as an important heterochromatin-euchromatin boundary in plants.
2020-12-02 | GSE127665 | GEO
Project description:How heterochromatin genes evolve as ‘gene islands’ to fit into the repressive chromatin environment in plants are poorly understood. To address this question, we performed a comprehensive epigenetic profiling in the genus Oryza with high quality BAC-assembled regional sequences and near gap-free genomes. Comparative analyses of a heterochromatin knob demonstrated the dynamics of chromatin states (heterochromatin versus euchromatin) among the Oryza species in a phylogenetic context. LTR (long-terminal repeat) retrotransposons are the main contributor (~99%) to heterochromatin diversity. Heterochromatin genes are distributed as ‘gene islands’ in heterochromatin, but heterochromatin hardly projects expression disturbance to them. Heterochromatin genes are almost free of H3K9me2 histone modifications in exons, and have similar gene structure and transposon invasion rate in introns to its orthologous euchromatin counterparts. Analyses of the rice HiC data verified the topological existence of ‘gene islands’ and demonstrated that ‘gene islands’ are less spatially co-localized with heterochromatin. By examining evolutionarily recent inserted genes in the Oryza species, we found that the active promoters of six inserted genes can elevate CHH (H=A, C, T) methylation at the insertion sites. Our results reveals that heterochromatin genes evolve as heterochromatin-insulated ‘gene islands’ to escape the repressive influence of heterochromatin, contrasting to the ‘integration’ model in Drosophila. We suggest that active gene promoters may contribute to this insulation by acting as an important heterochromatin-euchromatin boundary in plants.
2020-12-02 | GSE126432 | GEO