Transcriptome analysis upon Sin3A or Sam-S knockdown or both in Drosophila cultured S2 cells
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ABSTRACT:
PROVIDER: PRJNA530234 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8832530_1.fastq.gz | Fastqsanger.gz | |||
| SRR8832530_2.fastq.gz | Fastqsanger.gz | |||
| SRR8832540_1.fastq.gz | Fastqsanger.gz | |||
| SRR8832540_2.fastq.gz | Fastqsanger.gz | |||
| SRR8832531_1.fastq.gz | Fastqsanger.gz |
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Project description:The SIN3 histone modifying complex regulates the expression of multiple methionine catabolic genes including SAM synthetase (Sam-S) as well as the level of S-adenosyl-methionine (SAM). To further investigate the relationship between methionine catabolism and epigenetic regulation by SIN3, we identified genes controlled by SIN3 and SAM-S. As a global transcriptional regulator, SIN3 impacted a wide range of genes. Independently, SAM-S affected a narrow range of genes. Additional genes, however, were influenced in dual knockdown cells. At some genes, SIN3 and SAM-S act independently, for others, redundantly and for a third set, in opposition. Together, the results obtained in the study of SIN3, a cofactor associated with histone modification, and SAM-S, a metabolic enzyme, uncover a complex relationship on regulating transcription.
2019-11-26 | GSE129145 | GEO
Project description:SIN3 the scaffold protein of a histone deacetylase complex interacts with a histone demethylase KDM5 (little imaginal discs - LID) in Drosophila. Reduction of SIN3 or dKDM5/LID both result in similar phenotypes during cell proliferation and wing development. To identify underlying transcriptional changes that may contribute to these phentypic defects we performed whole genome expression analysis in Drosophila cultured cells upon RNAi-mediated knockdown of Sin3A, lid or both. We identified a large number of genes regulated by SIN3, dKDM5/LID or both. While many common genes were regulated by SIN3 and dKDM5/LID an enrichment for genes involved in stress tolerance pathways was observed. Additional RNAseq analysis of expression changes upon knockdown of Sin3A, lid or both under paraquat mediated oxidative stress conditions identified significant changes in genes involved in cell cycle related processes. Drosophila S2 cells were treated with dsRNA targetting Sin3A, lid and both or GFP as control under normal or oxidative stress conitions induced by treatment with paraquat. mRNA profiling of these samples were performed by deep sequencing using Illumina Hiseq2500.Three biological replicates were performed.
2016-01-09 | E-GEOD-68775 | biostudies-arrayexpress
Project description:SIN3 the scaffold protein of a histone deacetylase complex interacts with a histone demethylase KDM5 (little imaginal discs - LID) in Drosophila. Reduction of SIN3 or dKDM5/LID both result in similar phenotypes during cell proliferation and wing development. To identify underlying transcriptional changes that may contribute to these phentypic defects we performed whole genome expression analysis in Drosophila cultured cells upon RNAi-mediated knockdown of Sin3A, lid or both. We identified a large number of genes regulated by SIN3, dKDM5/LID or both. While many common genes were regulated by SIN3 and dKDM5/LID an enrichment for genes involved in stress tolerance pathways was observed. Additional RNAseq analysis of expression changes upon knockdown of Sin3A, lid or both under paraquat mediated oxidative stress conditions identified significant changes in genes involved in cell cycle related processes.
2016-01-09 | GSE68775 | GEO
Project description:4C-seq analysis using three viewpoint sequences in the Drosophila Bithorax Complex of Hox genes. 4C contacts were compared among S2 cells and those expressing wild type or SAM mutant Ph.
2015-12-01 | GSE61115 | GEO
Project description:Sin3a is the central scaffold protein of the prototypical Hdac1/2 chromatin repressor complex, crucially required during early embryonic development for the growth of pluripotent cells of the inner cell mass. Here, we explore the endogenous composition of the Sin3a-Hdac complex in pluripotent embryonic stem (ES) and differentiated cells. To do this, we established an endogenous double immunoprecipitation strategy coupled with quantitative mass spectrometry (ENDIP-MS) allowing us to define the precise composition of the Sin3a complex in multiple cell types. We identify the Fam60a subunit as a key defining feature of a variant Sin3a complex present in ES cells, but not in differentiated cells. Fam60a co-occupies H3K4me3 positive promoters with Sin3a and is essential to maintain it on chromatin. Consistent with this, Fam60a depletion phenocopies the loss of Sin3a, leading to decreased proliferation, an extended G1-phase and the deregulation of genes associated with differentiation. Taken together, our data characterise Fam60a as an essential core subunit of a variant Sin3a complex in ES cells required to promote rapid proliferation and to prevent unscheduled differentiation.
2017-05-19 | PXD005464 | Pride
Project description:SIN3 is a master transcriptional scaffold protein. SIN3 interacts with RPD3 and other accessory proteins to form a histone modifying complex. A single Sin3A gene encodes multiple isoforms of SIN3, of which SIN3 187 and SIN3 220 are the predominant isoforms. Previous studies demonstrated that SIN3 isoforms play non-redundant roles during fly development. In the current study, we sought to investigate the genes regulated by SIN3 187. S2 cells and cells carrying a stable transgene of SIN3 187HA (SIN3 187HA cells) were treated with 0.07 µM CuSO4. CuSO4 treatment led to ectopic expression of SIN3 187HA. S2 cells were used as a control. Following induction, total mRNA was extracted. mRNA profiling of these samples were performed by deep sequencing using Illumina Hiseq2500. Three biological replicates were performed.
2016-01-09 | E-GEOD-72172 | biostudies-arrayexpress
Project description:Tyrosine phosphorylation is a hallmark for activation of Signal Transducer and Activator of Transcription (STAT) proteins, but their transcriptional activity also depends on other secondary modifications. Type I interferons (IFNs) can activate both the ISGF3 (STAT1:STAT2:IRF9) complex and STAT3, but with cell-specific, selective triggering of only the ISGF3 transcriptional program. Following a genome-wide RNAi screen, we identified the Sin3a complex as an important mediator of this STAT3 transcriptional repression. Sin3a directly interacts with the DNA-binding domain of STAT3 and alters its acetylation status. SIN3A silencing enhances recruitment of STAT3 and enhanceosome components to the SOCS3 promoter, resulting in histone hyperacetylation and enhanced transcription. Conversely, Sin3a is required for ISGF3-dependent gene transcription and for an efficient IFN-mediated antiviral protection against Influenza A and hepatitis C viruses. The Sin3a complex therefore acts as a context-dependent STAT1/3 transcriptional switch. MCF7 cells were transfected with 50nM Renilla luciferase (control) or SIN3A-specific siRNA. 72h later, cells were cultured for 4h in absence of FCS and left non-stimulated or stimulated with LIF (10ng/ml, 1h). Total RNA was extracted. For each of the 4 conditions, 3 biological replicates were included. Nevertheless, one sample (SIN3A_siRNA_LIF1h_rep3) was discarded. In total 11 samples were analyzed.
2012-08-01 | E-GEOD-35696 | biostudies-arrayexpress
Project description:Tyrosine phosphorylation is a hallmark for activation of Signal Transducer and Activator of Transcription (STAT) proteins, but their transcriptional activity also depends on other secondary modifications. Type I interferons (IFNs) can activate both the ISGF3 (STAT1:STAT2:IRF9) complex and STAT3, but with cell-specific, selective triggering of only the ISGF3 transcriptional program. Following a genome-wide RNAi screen, we identified the Sin3a complex as an important mediator of this STAT3 transcriptional repression. Sin3a directly interacts with the DNA-binding domain of STAT3 and alters its acetylation status. SIN3A silencing enhances recruitment of STAT3 and enhanceosome components to the SOCS3 promoter, resulting in histone hyperacetylation and enhanced transcription. Conversely, Sin3a is required for ISGF3-dependent gene transcription and for an efficient IFN-mediated antiviral protection against Influenza A and hepatitis C viruses. The Sin3a complex therefore acts as a context-dependent STAT1/3 transcriptional switch.
2012-08-02 | GSE35696 | GEO
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