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Gene expression in HeLa cells expressing GFP-IRF3 (non-targeting control and clonal knockouts of DDX58, MAVS, ATP13A1, CAPN15, TADA2B, MED16, and MED24) following Sendai virus (SeV) infection or hpRNA transfection

ABSTRACT: IRF3 translocates from the cytoplasm to the nucleus upon recognition of a cytoplasmic RNA stimulus by RIG-I or MDA5. Using an optical pooled CRISPR knockout screen in HeLa-Cas9 cells, we identified ATP13A1, CAPN15, TADA2B, MED16, and MED24 as novel genes affecting the translocation of IRF3 upon Sendai virus infection. We generated isogenic clonal knockout HeLa-Cas9 lines and confirmed that loss of these five novel genes results in either decreased (ATP13A1 and CAPN15) or increased (TADA2B, MED16, and MED24) translocation of IRF3 upon Sendai virus or synthetic hpRNA stimulation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179288 | GEO | 2023/03/05

REPOSITORIES: GEO

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Gene expression in HeLa cells expressing GFP-IRF3 (non-targeting control and clonal knockouts of DDX58, MAVS, ATP13A1, CAPN15, TADA2B, MED16, and MED24) following Sendai virus (SeV) infection or hpRNA transfection

Project description:Gene expression in HeLa cells expressing GFP-IRF3 (non-targeting control and clonal knockouts of DDX58, MAVS, ATP13A1, CAPN15, TADA2B, MED16, and MED24) following Sendai virus (SeV) infection or hpRNA transfection

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Timecourse of gene expression in HeLa cells (parental cells and clonal knockouts of MED12 and MED24) following induction by TNFa or IL-1b

Project description:Activation of nuclear factor kappa B (NF-kB) by inflammatory signals results in nuclear translocation of the transcription factor p65 and induction of gene expression. We identified MED12 and MED24 in an optical pooled CRISPR knockout screen in HeLa-Cas9 cells for genes affecting the activation and/or relaxation of p65 to the cytoplasm following induction by either TNFa or IL-1b. We generated isogenic clonal knockout HeLa-Cas9 lines using crRNA transfection and confirmed that loss of MED12 or MED24 results in delayed relaxation of p65, assayed by live-cell imaging of a p65-mNeonGreen fluorescent fusion.

2019-10-01 | GSE132704 | GEO

Mismatch hpRNA prevents intrinsic self-silencing and enhances RNAi stability

Project description:Hairpin RNA (hpRNA) transgenes, with a perfect inverted-repeat (IR) DNA, have been the most successful RNA interference (RNAi) method in plants. Here we show that hpRNA transgenes were invariably methylated in the IR DNA and the adjacent promoter, causing transcriptional self-silencing and preventing the full potential of RNAi. Nucleotide substitutions in the sense sequence, which disrupts the perfect IR DNA structure, were sufficient to prevent the intrinsic DNA methylation resulting in more uniform and persistent RNAi. Substituting all cytosine (C) with thymine (T) nucleotides, in a G:U hpRNA design, prevented DNA methylation and self-silencing but still allowed for the formation of perfect hpRNA due to G:U wobble base-pairing. The G:U design induces effective RNAi in 90-96% of transgenic lines, compared to 57-65% for the traditional hpRNA design. Furthermore, while a traditional hpRNA transgene showed increasing DNA methylation and self-silencing from cotyledons to true leaves, the G:U transgenes avoided this developmental progression of self-silencing and induced RNAi throughout plant growth. The G:U and traditional hpRNA transgenes generated small interfering RNA (siRNA) with different 5’ phosphorylation, which resembled the endogenous tasiRNA and miRNA, respectively. Furthermore, our results suggest that siRNAs from the two transgene designs function differently to induce target DNA methylation, one (from traditional hpRNA) through the canonical RdDM pathway and the other (G:U hpRNA) a non-canonical pathway. Our study not only revealed a methylation-resistant RNAi transgene design but also provided new mechanistic insights into small RNA biogenesis and function in plants

2022-03-31 | GSE178565 | GEO

Specific silencing of pathogenic mRNA by a novel compact RNA-targeting tool TaqTth-hpRNA

Project description:Pathogenic allele silencing is a promising treatment for genetic hereditary diseases. However, the concern about the specificity of present RNA-knockdown strategies has limited their in vivo applications. Here a TaqTth-hpRNA system consisting of a small, chimeric protein (TaqTth) and hairpin-RNA probe (hpRNA) is provided. The TaqTth-hpRNA showed a high-specific knockdown against targeted mRNA with minimal flanking sequence-motif requirement and less cell viability damage, then was applied to mutant APPswe mRNA silencing without altering the wild-type APP mRNA in Alzheimer’s disease. Notably, the combination of the TaqTth and human apolipoprotein E 2 (APOE2) overexpression encoded in a single AAV vector is available due to the compact size of TaqTth, and showed stronger inhibition of pathologies in the mouse model. Altogether, we provided the basis for a small RNA-targeting tool with high selectivity, minimal flanking sequence-motif requirement, less cell viability damage and potentially being an alternative in therapeutic applications.

2024-06-30 | GSE236392 | GEO

Genome-wide gene expression analysis of FAF1 silencing in HeLa cells

Project description:This study is designed to examine the cellular functions of human Fas-associated factor 1 (FAF1) containing multiple ubiquitin-related domains. Microarray analyses revealed that interferon stimulated genes related to antiviral response are significantly increased in FAF1 knocked down HeLa cells. Silencing FAF1 enhanced the poly I:C and respiratory syncytial virus (RSV) induced productions of type I interferons (IFNs), the target gene of interferon regulator factor 3 (IRF3). IRF3 is a key transcription factor in IFNβ signaling responsible for host innate immune response. This study also found that FAF1 and IRF3 physically associate with IPO5/importin-β3 and that overexpression of FAF1 reduces the interaction between IRF3 and IPO5/importin-β3. These findings suggest that FAF1 negatively regulates IRF3-mediated IFNβ production and antiviral innate immune response via regulating nuclear translocation of IRF3. We conclude that FAF1 plays a novel role negatively regulating virus-induced IFNβ production and antiviral response by inhibiting the translocation of active phosphorylated IRF3 from cytosol to nucleus.

2016-01-29 | GSE71665 | GEO

Specific silencing of pathogenic mRNA by a novel compact RNA-targeting tool TaqTth-hpRNA [Amplicon sequencing]

2024-06-20 | GSE269593 | GEO

Specific silencing of pathogenic mRNA by a novel compact RNA-targeting tool TaqTth-hpRNA [RNA-seq]

2024-06-20 | GSE269592 | GEO

Mismatch hpRNA prevents intrinsic self-silencing and enhances RNAi stability

Project description:Mismatch hpRNA prevents intrinsic self-silencing and enhances RNAi stability

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IRF3 prevents colorectal tumorigenesis via inhibiting the nuclear translocation of β-catenin

Project description:Occurrence of Colorectal cancer（CRC）is relevant with gut microbiota. However, role of IRF3, a key signaling mediator in innate immune sensing, has been barely investigated in CRC. Here, we unexpectedly found that the IRF3 deficient mice are hyper-susceptible to the development of intestinal tumor in AOM/DSS and Apcmin/+ models. Genetic ablation of IRF3 profoundly promotes the proliferation of intestinal epithelial cells via aberrantly activating Wnt signaling. Mechanically, IRF3 in resting state robustly associates with the active β-catenin in the cytoplasm, thus preventing its nuclear translocation and cell proliferation, which can be relieved upon microbe-induced activation of IRF3. In accordance, the survival of CRC is clinically correlated with the expression level of IRF3. Therefore, our study identifies IRF3 as a negative regulator of the Wnt/β-catenin pathway and a potential prognosis marker for Wnt-related tumorigenesis, and describes an intriguing link between gut microbiota and CRC via the IRF3-β-catenin axis.

2020-09-16 | GSE155777 | GEO

Gene expression in IRF3-/- peritoneal macrophage infected with VSV

Project description:IRF3 is one of the most critical transcription factor in down stream of pattern recognition receptors (such as toll-like receptor and RIG-I-like receptor) signalling pathway. IRF3 is known to induce the expression of type I IFN gene upon virus infection. To furter examine the role of IRF3 in virus-induced gene expression, we preformed microarray analysis in IRF3-/- peritoneal macrophages infected with VSV, and found that IRF3 suppresses the expression of Il12b gene. Peritoneal macrophages from WT of IRF3-/- B6 mice were infected with VSV(1 M.O.I. ) for 6 hous, and then subjected to microarray analysis.

2012-05-19 | E-GEOD-37855 | biostudies-arrayexpress

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