Transcriptomics changes after IFN-alpha2 treatment following dBRD9-A or DMSO pretreatment in A549 lung epithelial cells
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ABSTRACT:
PROVIDER: PRJNA739760 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14875248.fastq.gz | Fastqsanger.gz | |||
| SRR14875249.fastq.gz | Fastqsanger.gz | |||
| SRR14875250.fastq.gz | Fastqsanger.gz | |||
| SRR14875251.fastq.gz | Fastqsanger.gz | |||
| SRR14875252.fastq.gz | Fastqsanger.gz |
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Project description:These experiments aim at defining first the entirety of Interferon-stimulated gene expression in A549 in response to treatment with 100 IU/mL IFN-alpha2. The second second aim was to characterize changes to the transcriptome caused by the prior degradation of bromodomain-containing protein9 (BRD9) by the use of a specific BRD9-degrader (dBRD9-A) both in the uninduced and IFN-alpha2-induced conditions.
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Project description:BRD9 was identified in a genome-wide screen for genes regulating the response to interferon (IFN) in a A549 based reporter cell line. Subsequent experiments determined an involvement of BRD9 in the transcriptional regulation of Interferon-stimulated genes (ISGs) expression following stimulation with IFN-a2. The aim of this proximity-labelling experiments was to gain a more mechanistic understanding of BRD9 recruitment during the IFN signal transduction using A549 cells stably transduced with BRD9-TurboID and mCherry-TurboID fusion proteins. The BRD9 interactome in the absence of IFN- a2 was determined. We found that following IFN-a2 treatment, STAT2 significantly associates with BRD9-TurboID.
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Project description:Type-II interferon or IFN-gamma is a critical cytokine in innate immunity that control multitude of intracellular infections. IFN-gamma binds to interferon gamma receptors to phosphorylate and activate STAT1 mediated transcription of interferon stimulated genes (ISGs). We executed a genome-wide CRISPR-Cas9 screen against ~20,000 human genes to identify IRF-1 and NF2 as significant regulators of Toxoplasma infection in A549 lung epithelial cells. IRF-1 is a key transcription factor immediately downstream of STAT1 induced transcription that amplifies ISG expression in different cell types. NF2 or MERLIN is a tumor suppressor that is known to regulate expression of genes involved with cellular growth and metabolism. Transcriptomic signature of A549 cells lacking IRF-1 and NF2 were measured upon activation with IFN-gamma to find set of genes that may be regulating Toxoplasma infection. A total of 1,046,709,676 reads from 3 independent biological replicates were mapped to human hg38 reference genome. Expression of a ISGs that failed to induced in cells lacking IRF1 were found to be dysregulated in absence of NF2 as well.
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Project description:Type-I (e.g. IFN-alpha, IFN-beta) and type-II IFNs (IFN-gamma) have antiviral, antiproliferative, and immunomodulatory properties. Both types of IFN signal through the Jak/STAT pathway to elicit antiviral activity, yet IFN-gamma is thought to do so only through STAT1 homodimers while type-I IFNs activate both STAT1- and STAT2-containing complexes such as ISGF3. Here we show that ISGF3II - composed of phosphorylated STAT1, unphosphorylated STAT2, and IRF9 - also plays a role in IFN-gamma-mediated antiviral activity in humans. Using phosphorylated STAT1 as a marker for IFN signaling, western blot analysis of IFN-alpha2a treated human A549 cells revealed that pSTAT1 (Y701) levels peaked at 1h, decreased by 6h, and remained at low levels for up to 48h. Cells treated with IFN-gamma showed a biphasic pSTAT1 response with an early peak at 1-2h and a second peak at 15-24h. Gene expression microarray following IFN-gamma treatment for 24h indicated an induction of antiviral genes that are induced by ISGF3 and associated with a type-1 IFN response. Induction of these genes by autocrine type-I and type-III IFN signaling was ruled out using neutralizing antibodies to these IFNs in biological assays and by qRT-PCR. Despite the absence of autocrine IFNs, IFN-gamma treatment induced formation of ISGF3II. This novel transcription factor complex binds to ISRE promoter sequences, as shown by ChIP analysis of the PKR promoter. STAT2 and IRF9 knockdown in A549 cells reversed IFN-gamma-mediated ISRE induction and antiviral activity - implicating ISGF3II formation as a significant component of the cellular response and biological activity of IFN-gamma. Two treatments using three biological replicates each were performed using three million A549 cells. Each was seeded overnight in 10mL complete RPMI and treated. Three were treated with alpha-IFN and three treated with gamma-IFN for 24h. Control samples were left untreated.
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Project description:Ferroptosis is a new type of programmed cell death induced by iron-dependent lipid peroxidation that has been linked to several malignancies, including non-small cell lung cancer (NSCLC). Finding ferroptosis-associated genes is extremely helpful for guiding and improving ferroptosis-based anti-tumor therapy. To explore ferroptosis-associated genes, we treated A549 cells with DMSO, RSL3 alone, or co-treated with Fer-1 for 24h. Lung cancer-associated transcript 1 (LUCAT1) was identified as a novel ferroptosis suppressor via RNA-seq analysis.
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