Characterization of the transcriptional response to DNA in STING KO cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA531319 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8863220.fastq.gz | Fastqsanger.gz | |||
| SRR8863230.fastq.gz | Fastqsanger.gz | |||
| SRR8863240.fastq.gz | Fastqsanger.gz | |||
| SRR8863211.fastq.gz | Fastqsanger.gz | |||
| SRR8863221.fastq.gz | Fastqsanger.gz |
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Project description:HEK-Blue™ ISG Cells and HEK-Blue™ ISG-KO-STING Cells (Invivogen) were transfected with dacA (Listeria monocytogenes) for 12 and 24 hours. Through this approach, we described the STING-dependent and STING-independent transcriptional response to dacA. Our analysis reveals a STING-dependent enrichment of interferon stimulated genes beginning 12 hours post-transfection, and a STING-independent enrichment of genes associated with protein translation and oxidative phosphorylation.
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Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type (WT), Trex1 deficient (TKO), STING deficient (SKO), or Trex1 and STING double deficient (STKO) mouse Heart
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Project description:RNA-Sequencing of STING competent and STING-KO cells after transfection with dacA (Listeria monocytogenes)
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Project description:The aim of this study was to identify the signaling pathways differentially engaged upon infection with either live or heat killed Mycobacterium tuberculosis in murine bone marrow derived macrophages. Based on preliminary data that type I IFN signaling dominates the transcriptional differences, we investigated what roles the type I IFN receptor IFNAR and the signaling molecule STING play during infection with either live or heat killed Mycobacterium tuberculosis in bone marrow derived macrophages. In WT and STING KO macrophages, IFNbeta treatment was added either by itself or in addition to both of the infection conditions to test whether the lack of IFNbeta induction in these cells accounted for any differences in transcriptional respones.added IFNbeta treatment either by itself or in addition to both of the infection conditions.
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Project description:The STING signaling pathway plays important roles in many cancers, viral and bacterial infections, and autoimmune diseases. Understanding how STING mediates expression of many proteins in the host and bacterial cells can provide important clues about the biochemical processes, opening the door for the development of new therapies. Using STING KO cells, we were able to identify many differentially expressed proteins between the wild type and STING KO RAW macrophage. We identified proteins that were exclusively detected only in the wild type or only in the STING KO, as well as those that were comply identified but showed different levels of expressions between the two cell lines. This included several proteins that are known as potent biomarkers of various cancers and autoimmune diseases. Our data broaden the knowledge of proteins that are related to STING signaling, and may have identified novel proteins that have therapeutic value. This will require rigorous validation in the future studies. Many protein biomarkers can be regulated by post-translational modifications and protein-protein interactions. While beyond the scope of the current study, we note that methods are available at the Purdue Proteomics Facility for mapping post-translational modifications and protein-protein interactions. We envision this to be an exciting line of enquiry for us in the future.
2019-07-03 | MSV000084058 | MassIVE
Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), Trex1 deficient MEFs (TKO) or STING and Trex1 double deficient MEFs (STKO) transfected with or without double strand DNA 90 (ISD) and examined cytokine production by these cells.
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Project description:We report positional cloning and characterization of a novel Sting allele that fails to activate IFN production in the wild-derived mice of MOLF/Ei strain in response to HSV (Herpes Simplex Virus) and Listeria monocytogenes both in vitro and in vivo. We show that previously uncharacterized mutations in the N-terminal of STING are responsible for low levels of IFN due to failure of MOLF STING to respond to cytosolic STING agonists such as 2â3âcGAMP, 5,6-Dimethylxanthenone-4-acetic acid (DMXAA) or poly(deoxyadenylic-deoxythymidylic) acid (dAdT). Using Next-Generation Sequencing (NGS) for the analysis of DNA-responses in congenic C57BL6.StingMOLF/MOLF (MOLF STING) mouse macrophages, we show that these mutations in MOLF/Ei discriminate in responses between different STING agonists. Macrophages from C57BL6.StingB6/B6¬ (B6 STING), or B6 STING expressing littermates were stimulated as a positive control for STING activation, and STING -/- (STING KO) macrophages served as a negative control. To examine differential gene regulation downstream of murine Tmem173 (STING) allelic variants. We stimulated macrophages from B6 mice congenic for MOLF STING; macrophages from B6 STING expressing littermates were stimulated as a positive control for STING activation, and STING -/- (STING KO) macrophages served as a negative control. One replicate of RNA-seq reads after each stimulation provided. Conditions are peritoneal macrophages from B6 congenic mice expressing: B6 STING, MOLF STING, or STING KO stimulated with 2â3âcGAMP, 5,6-Dimethylxanthenone-4-acetic acid (DMXAA), poly(deoxyadenylic-deoxythymidylic) acid (dAdT), or no treatment. This constitutes a total of 12 reads analyzed in this data set.
2016-07-05 | E-GEOD-68140 | biostudies-arrayexpress
Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), STING deficient MEFs (SKO), Trex1 deficient MEFs (TKO), and both STING and Trex1 deficient MEFs (STKO) treated with DMBA and examined cytokine production by these cells.
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