Ontology highlight
ABSTRACT:
PROVIDER: PRJNA259168 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1551870.fastq.gz | Fastqsanger.gz | |||
| SRR1555770.fastq.gz | Fastqsanger.gz | |||
| SRR1555771.fastq.gz | Fastqsanger.gz | |||
| SRR1555766.fastq.gz | Fastqsanger.gz | |||
| SRR1555767.fastq.gz | Fastqsanger.gz |
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Project description:Dicer and Hsp104 function in a negative feedback loop to confer epigenetic robustness [RNA_profiles]
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Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins. Various strains grown at 30°C or 37°C
2015-04-23 | E-GEOD-60638 | biostudies-arrayexpress
Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins. wt_spb75 grown at 30°C or 37°C
2015-04-23 | E-GEOD-60429 | biostudies-arrayexpress
Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins.
2015-04-23 | GSE60638 | GEO
Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins.
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Project description:Oncogene induced senescence (OIS) is a tumor suppressive mechanism typified by stable proliferative arrest, a persistent DNA damage response and the senescent-associated secretory phenotype (SASP). MacroH2A1, a tumor suppressive histone variant, is upregulated during OIS. Using ChIP-seq, we found that macroH2A1 undergoes dramatic relocalization during OIS. SASP genes are enriched in macroH2A1-containing chromatin and macroH2A1 is a critical component of the positive feedback loop that maintains SASP expression. Endoplasmic reticulum (ER) stress, a feature of OIS that requires macroH2A1, leads to ATM activation. ER stress triggers a negative feedback loop reducing SASP expression by causing the ATM-dependent removal of macroH2A1 from SASP genes. MacroH2A1 represents a critical control point in the regulation of SASP expression during OIS by We demonstrate that SASP gene expression is regulated by the combined actions of a positive feedback loop that requires macroH2A1 and a negative feedback loop where ER stress leads to ATM activation critical for the removal of macroH2A1 from SASP genes and consequently their repression.
2015-08-19 | GSE64601 | GEO
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2017-02-19 | GSE79357 | GEO
Project description:During hematopoiesis, cells originating from the same stem cell reservoir differentiate into distinct cell types. The mechanisms enabling common progenitors to differentiate into distinct cell fates are not fully understood. Here, we identify chromatin-regulating and cell-fate-determining transcription factors (TF) governing dendritic cell (DC) development by annotating the enhancer and promoter landscapes of the DC lineage. Combining these analyses with detailed over-expression, knockdown and ChIP-Seq studies, we show that Irf8 functions as a plasmacytoid DC epigenetic and fate-determining TF, regulating massive, cell-specific chromatin changes in thousands of pDC enhancers. Importantly, Irf8 forms a negative feedback loop with Cebpb, a monocyte-derived DC epigenetic fate-determining TF. We show that using this circuit logic, differential activity of TF can stably define epigenetic and transcriptional states, regardless of the microenvironment. More broadly, our study proposes a general paradigm that allows closely related cells with a similar set of signal-dependent factors to generate differential and persistent enhancer landscapes. Here we profiled accessible chromatin of moDC and pDC using ATAC-seq assay, developed by Buenrostro et al. (2013)
2014-12-14 | E-GEOD-62703 | biostudies-arrayexpress
Project description:The core miRNA biogenesis enzyme Dicer sustains recurrent mutations in cancer, which specifically compromise catalysis by its RNase IIIb domain. These are proposed to act as selective hypomorphs, since Dicer-RNase IIIb cleaves the 5p arms of pre-miRNA hairpins. However, the lack of knockin models has hindered a full understanding of the consequences of Dicer hotspot mutations for miRNA biogenesis. Here, we generated Dicer-KO and Dicer-S1344L (homozygous and hemizygous) hESCs; the latter is a non-catalytic mutation in RNase IIIa that impairs RNase IIIb activity. Consistent with our previous work, Dicer-KO is cell lethal in hESCs. However, in contrast to the expectation that Dicer hotspot mutations confer cell advantages, Dicer-S1344L knockin hESCs were subviable and also required a conditional genetic strategy for isolation. Small RNA sequencing using spike-in normalization reveals two broad trends: ablation of miRNA-5p species, and selective changes in miRNA-3p species. Curiously, we recognized a directional upregulation of miRNA-3p passenger strands, indicating a broad strand switch. Activity assays and Argonaute profiling of the transcriptome confirm that these confer increased repression capacity. Finally, we used in vitro assays to show 3p arm-nicked pre-miRNAs preferentially load miRNA-3p species into Argonaute, compared to corresponding miRNA/passenger duplexes. Overall, Dicer hotspot mutations have unexpected neomorphic consequences on miRNAs, including both loss- and gain-of-function.
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