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DNaseI hypersensitivity mapping/DNaseI high-throughput sequencing (DHS-Seq) in Saccharomyces cerevisiae

ABSTRACT: We report the application of DHS-Seq and digital genomic footprinting to study chromatin changes and transcription factor-DNA binding upon long-term Hsp90 depletion utilizing the temperature-sensitive allele G170D. By generating about 86 and 85.6 million reads for wild type and mutant, we were able to reconstitute the chromatin accessibility and the transcription factor-DNA binding maps under regular conditions and under conditions where Hsp90 was long-term inactivated. We find that there is a global reduction of transcription factor binding sites with concurrent loss of open chromatin upon Hsp90 inactivation. This data was used in conjunction with our previous work involving DHS-Seq studies and short-term Hsp90 depletion (GEO GSE88875) to distinguish the affected transcription factor networks and the chromatin changes upon short- and long-term Hsp90 depletion. We identified two different modes of Hsp90 operation on transcription factor activities – short-term inactivation of Hsp90 altered transcription factor DNA binding activities, whereas long-term Hsp90 inactivation affected the steady-state levels of transcription factors. Overall, this study shows that Hsp90 regulates multiple transcription factor protein families and modulates chromatin architecture on a genome-wide scale.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE139268 | GEO | 2019/10/23

REPOSITORIES: GEO

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Yeast Hsp90-dependent chromatin changes as monitored using DNase-Seq

Project description:We report the application of DNase-Seq (adapted from Hesselberth et al., 2009, as described in Zelin et al., 2012) to study the chromatin changes upon short Hsp90 depletion by exploiting temperature-sensitive allele G170D (Nathan and Lindquist, 1995). By generating ~43.6 million reads for wild type and 68.6 million reads for mutant, we were able to reconstitute the hypersensitivity maps under the regular conditions and under the conditions where Hsp90 was heat-inactivated. We find that there is a global reduction of open chromatin upon Hsp90 inactivation, as displayed by the decrease of total DHS size and the DHSs numbers. We also find that loss of Hsp90 leads to the increase of open chromatin at certain locations associated with chromatin remodelers such as RSC. Overall this study shows that short term improper functioning of Hsp90 results in genome-wide chromatin perturbations thereby demonstrating an Hsp90-dependence of chromatin architecture.

2016-11-03 | GSE88875 | GEO

RNA sequencing (RNA-Seq) in Saccharomyces cerevisiae

Project description:Genomic events including gene regulation and chromatin status are controlled by transcription factors. Here we report that the Hsp90 molecular chaperone broadly regulates the transcription factor protein family. Our studies identified a biphasic use of Hsp90 in which early inactivation (15 min) of the chaperone triggered a wide reduction of DNA binding events along the genome with concurrent changes to chromatin structure. Long-term loss (6 h) of Hsp90 resulted in a decline of a divergent yet overlaying pool of transcription factors that produced a distinct chromatin pattern. Although both phases involve protein folding, the early point correlated with Hsp90 acting in a late folding step that is critical for DNA binding function whereas prolonged Hsp90 inactivation led to a significant decrease in the steady-state transcription factor protein levels. Intriguingly, despite the broad chaperone-impact on a variety of transcription factors, the operational influence of Hsp90 was at the level of chromatin with only a mild effect on gene regulation. Thus, Hsp90 selectively governs the transcription factor process overseeing local chromatin structure.

2019-10-23 | GSE139266 | GEO

Changes in chromatin accessibility in mouse liver following TCPOBOP exposure

Project description:This work is part of a larger study where we investigated activation of the nuclear receptor and transcription factor CAR (Nr1i3) by its specific agonist ligand TCPOBOP (1,4-bis[2-(3,5-dichloropyridyloxy)]benzene), which dysregulates hundreds of genes in mouse liver and is linked to male-biased hepatocarcinogenesis. We used DNase-seq and DNase hypersensitivity site (DHS) analysis to identify several thousand genomic regions (∆DHS) where short-term exposure to TCPOBOP induces localized changes (increases or decreases) in mouse liver chromatin accessibility, many of which cluster together with TCPOBOP-responsive genes. Sites of chromatin opening were highly enriched nearby genes induced by TCPOBOP and chromatin closing was highly enriched nearby genes repressed by TCPOBOP, consistent with TCPOBOP-responsive ∆DHS serving as enhancers and promoters that positively regulate CAR-responsive genes. Gene expression changes lagged behind chromatin opening or closing for a subset of TCPOBOP-responsive ∆DHS. DHS that were specifically responsive to TCPOBOP in male liver were significantly enriched for genomic regions with a basal male bias in chromatin accessibility; however, the male-biased response of hepatocellular carcinoma-related genes to TCPOBOP was not associated with a correspondingly male-biased ∆DHS response. These studies elucidate the genome-wide organization of CAR-responsive genes and of the thousands of associated genomic sites where TCPOBOP exposure induces both rapid and persistent changes in chromatin accessibility.

2018-04-09 | GSE104061 | GEO

Time- and dose-resolved proteome of PM2.5 exposure in rat model

Project description:this paper used Mass spectrometry, Fast-seq, and catTFRE to study the pattern of 6316 proteins as well as 387 Transcription factors associated with PM2.5 in both short-term and long-term rat injury models.

2020-05-27 | PXD019404 | iProX

Expression data from WT and GABPalpha-deficient Flt3(-) LSK cells

Project description:GABPalpha is an Ets family transcription factor and involved in regulation of both basic cellular functions such as cell cycle progression and tissue-specific biological processes. We found that GABPalpha is critically required for survival and differentiation of hematopoietic stem cells. We used microarrays to detect gene expression changes in Flt3(-) LSK cells (which contains both long-term and short-term hematopoietic stem cells) by GABPalpha deficiency. Mx1Cre-GABPa(FL/+) and Mx1Cre-GABPa(FL/-) mice were treated with pIpC to induce inactivation of GABPalpha in bone marrow cells. Four days after last treatment of pIpC, the bone marrow cells were isolated and the Flt3(-)LSK subset was purified by cell sorting. RNA was extracted and hybridized to GeneChip Mouse GENE 1.0 ST arrays (Affymetrix).

2011-07-27 | E-GEOD-23341 | biostudies-arrayexpress

Evolution of diapause in the African killifish by remodeling ancient gene regulatory landscape

Project description:Suspended animation (e.g. hibernation, diapause) allows organisms to survive extreme environments. But the mechanisms underlying the evolution of suspended animation states are unknown. The African turquoise killifish has evolved diapause as a form of suspended development to survive the complete drought that occurs every summer. Here, we show that gene duplicates – paralogs – exhibit specialized expression in diapause compared to normal development in the African turquoise killifish. Surprisingly, paralogs with specialized expression in diapause are evolutionarily very ancient and are present even in vertebrates that do not exhibit diapause. To determine if evolution of diapause is due to the regulatory landscape rewiring at ancient paralogs, we assessed chromatin accessibility genome-wide in fish species with or without diapause. This analysis revealed an evolutionary recent increase in chromatin accessibility at very ancient paralogs in African turquoise killifish. The increase in chromatin accessibility is linked to the presence of new binding sites for transcription factors, likely due to de novo mutations and transposable element (TE) insertion. Interestingly, accessible chromatin regions in diapause are enriched for lipid metabolism genes, and our lipidomics studies uncover a striking difference in lipid species in African turquoise killifish diapause, which could be critical for long-term survival. Together, our results show that diapause likely originated by repurposing pre-existing gene programs via recent changes in the regulatory landscape. This work raises the possibility that suspended animation programs could be reactivated in other species for long-term preservation via transcription factor remodeling and suggests a mechanism for how complex adaptations evolve in nature.

2021-08-05 | ST001898 | MetabolomicsWorkbench

Correlation between DNase I hypersensitive site distribution and gene expression in HeLa S3 cells [DNase-Hypersensitivity]

Project description:Mapping DNase I hypersensitive sites (DHSs) within nuclear chromatin is a traditional and powerful method of identifying genetic regulatory elements. DHSs have been mapped by capturing the ends of long DNase I-cut fragments (>100,000 bp), or 100-1200 bp DNase I-double cleavage fragments (also called double-hit fragments). But next generation sequencing requires a DNA library containing DNA fragments of 100-500bp. Therefore, we have modified the double-hit method and use short DNA fragments to generate DNA libraries for next generation sequencing. We call this method Short DHS Assay (Short DNAse I Hypersensitive Site assay). The short segments are 100-300bp and can be directly cloned and used for high-throughput sequencing. We identified 83,897 DHSs in 2,343,479 tags across the human genome. Our results indicate that the DHSs identified by the Short DHS assay are consistent with those identified by longer fragments in previous studies.

2015-06-19 | GSE38914 | GEO

Reprogramming of transcriptome after hormetic heat stress by the endoribonuclease ENDU 2 improves lifespan and stress resistance in C. elegans

Project description:Organisms' ability to respond to life-threatening environmental impacts is crucial for their survival. While acute stress responses to unfavorable factors are well known, the physiological consequences of transient stress experiences over time, as well as their underlying mechanisms, are not well understood. In this study, we investigated the long-term effects of a short heat shock (HS) exposure on the transcriptome of C. elegans. We found that the canonical HS response was followed by a profound transcriptional reprogramming affecting many genes involved in innate immunity response. This reprogramming relies on the endoribonuclease ENDU-2 but not the heat shock factor 1 (HSF-1). ENDU-2 in this context co-localizes with chromatin and interacts with RNA polymerase Pol II, enabling specific regulation of transcription in the post-HS period. Failure to activate this post-HS response does not impair animal survival under continuous HS insult but eliminates the beneficial effects of hormetic HS. In summary, our work discovers that the RNA-binding protein ENDU-2 mediates the hormetic long-term effects of transient HS to determine aging and longevity.

2023-06-29 | PXD041872 | Pride

Low-C on Human CB-derived LT-HSC and ST-HSC

Project description:Low-C was performed upon human cord-blood long-term hematopoietic stem cells (LT-HSC) and short-term hematopoietic stem cells (ST-HSC). This was used to demonstrate that chromatin conformation changes associated with LT-HSC activation are enriched in ST-HSC.

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Super-enhancer redistribution as a mechanism of broad gene dysregulation in repeatedly drug-treated cancer cells [dataset 2]

Project description:We provide a series of chromatin and transcriptomic profiles to establish the short-term and long-term effects of cisplatin treatment in ovarian cancer A2780 cells.

2020-04-01 | GSE129701 | GEO

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