Expression data in dSTING knockdown and control sibling flies after mock or pathogenic infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE54833 | GEO | 2015/09/22
SECONDARY ACCESSION(S): PRJNA237780
REPOSITORIES: GEO
Similar Datasets
Project description:Parental flies (y1v1;P{TRiP.JF01138}attP2 and y1w*;P{Act5C-GAL4}25FO1/CyO,y+) were mated to obtain progeny with genotypes for ubiquitous DmSTING RNAi and sibling controls. 2-7 day old flies were used for all infections. 23 nl of listeria monocytogenes (strain 10403S) at 1e7 CFU/ml was injected intrathoracically. Mock inoculation was performed with PBS. Whole flies were homogenized 24 h post-infection.
2018-06-19 | GSE90442 | GEO
Project description:The fruit fly Drosophila melanogaster is a good model to unravel the molecular mechanisms of innate immunity, and has led to some important discoveries on the sensing and signalling of microbial infections. The response of drosophila to virus infections remains poorly characterized, and appears to involve two facets. On one hand RNA interference (RNAi) involves the recognition and processing of dsRNA into small interfering (si) RNAs by the host ribonuclease Dicer-2 (Dcr-2), whereas on the other hand an inducible response controlled by the evolutionarily conserved JAK/STAT pathway contributes to the antiviral host defence. In order to clarify the contribution of the siRNA and JAK/STAT pathways to the control of viral infections, we have compared the resistance of flies wild-type or mutant for Dcr-2 or the JAK kinase Hopscotch (Hop) to infections by seven RNA or DNA viruses belonging to different families. Our results reveal a unique susceptibility of hop mutant flies to infection by DCV and CrPV, two members of the Dicistroviridae family. Genome-wide microarray analysis confirmed that different sets of genes were induced following infection by DCV (GSE2828) or two unrelated RNA viruses, FHV and SINV. Overall, our data reveal that RNAi is an efficient antiviral mechanism, operating against a large range of viruses, including a DNA virus. By contrast, the antiviral contribution of the JAK/STAT pathway appears to be virus-specific. For each experimental challenge (FHV, 48 or 72 hours after infection; SINV, 4 or 8 days after infection), three biologically independent samples composed of 45 male Oregon R flies were used. Infection has been performed by injecting viral stocks prepared in Tris solution. Injection of the same volume of Tris has been used as control. Infected flies were then incubated for 48 or 72 hours in the case of FHV and 4 days or 8 days in the case of SINV.
2013-02-06 | E-GEOD-31542 | biostudies-arrayexpress
Project description:The aim of the study was to generate transcriptome of wild-type and G9a mutant adult flies (females) 24h post-infection with Drosophila C Virus (DCV).
2015-01-24 | GSE56013 | GEO
Project description:To test whether other genes were being silenced in the Cyp6g1 knockdown strain due to off-target RNAi effects, and whether other gene expression changes were contributing to the altered susceptibility to imidacloprid in these knockdown flies. A comparison between w;Act5C-GAL4/CyO; UAS:RNAi_Cyp6g1Hp2/TM3Sb and the genetic control w;Act-GAL4/CyO;+/TM3Sb was performed. Ten 2-3 day old adult males or females were transferred to sugar-agar plates and then collected at various time points (0, 2, 5, 8 hours). The RNA samples for up to three independent experiments per timepoint for each genotype were then pooled, in equal concentrations, before hybridisation to the Affymetrix Drosophila GeneChip 1. As a preliminary analysis provided evidence for assuming that there is no interaction between genotype and duration in the sugar-agar plate, the knockdown and control chips for each of the five timepoints provided some degree of replication for the comparison between the knockdown flies and control flies. Differential expression that was consistently observed between knockdown and control over each of the five timepoints was regarded as providing evidence of a genuine difference.
2011-02-17 | GSE27344 | GEO
Project description:The fruit fly Drosophila melanogaster is a good model to unravel the molecular mechanisms of innate immunity, and has led to some important discoveries on the sensing and signalling of microbial infections. The response of drosophila to virus infections remains poorly characterized, and appears to involve two facets. On one hand RNA interference (RNAi) involves the recognition and processing of dsRNA into small interfering (si) RNAs by the host ribonuclease Dicer-2 (Dcr-2), whereas on the other hand an inducible response controlled by the evolutionarily conserved JAK/STAT pathway contributes to the antiviral host defence. In order to clarify the contribution of the siRNA and JAK/STAT pathways to the control of viral infections, we have compared the resistance of flies wild-type or mutant for Dcr-2 or the JAK kinase Hopscotch (Hop) to infections by seven RNA or DNA viruses belonging to different families. Our results reveal a unique susceptibility of hop mutant flies to infection by DCV and CrPV, two members of the Dicistroviridae family. Genome-wide microarray analysis confirmed that different sets of genes were induced following infection by DCV (GSE2828) or two unrelated RNA viruses, FHV and SINV. Overall, our data reveal that RNAi is an efficient antiviral mechanism, operating against a large range of viruses, including a DNA virus. By contrast, the antiviral contribution of the JAK/STAT pathway appears to be virus-specific.
2013-02-06 | GSE31542 | GEO
Project description:To test whether other genes were being silenced in the Cyp6g1 knockdown strain due to off-target RNAi effects, and whether other gene expression changes were contributing to the altered susceptibility to imidacloprid in these knockdown flies. A comparison between w;Act5C-GAL4/CyO; UAS:RNAi_Cyp6g1Hp2/TM3Sb and the genetic control w;Act-GAL4/CyO;+/TM3Sb was performed. Ten 2-3 day old adult males or females were transferred to sugar-agar plates and then collected at various time points (0, 2, 5, 8 hours). The RNA samples for up to three independent experiments per timepoint for each genotype were then pooled, in equal concentrations, before hybridisation to the Affymetrix Drosophila GeneChip 1. As a preliminary analysis provided evidence for assuming that there is no interaction between genotype and duration in the sugar-agar plate, the knockdown and control chips for each of the five timepoints provided some degree of replication for the comparison between the knockdown flies and control flies. Differential expression that was consistently observed between knockdown and control over each of the five timepoints was regarded as providing evidence of a genuine difference. 2-3 day old adult flies of the appropriate genotype (Cyp6g1 knockdown or its genetic control) were transferred to bioassay plates and collected after specified timepoints in the assay plate, i.e. 0, 2, 5 or 8 hours. Each experiment contained ?3 replicates of each genotype/timepoint, and a different number of independent experiments (1-3) were pooled per microarray sample as described below. An experiment is defined as treatments set up from the same cohort of flies on a single day. Independent experiments are set up using distinct cohorts of flies, on distinct days. We included one pair of tests to compare samples from single experiments with pooled samples from independent experiments (DS003001 to DS003004, DS003002 to DS003005), and also a single pair of samples to compare males to females (DS003002 to DS003003). As it turned out - in our analysis - the timepoints selected were not discriminative, in that there were no differences detected that could be attributed to an effect of time in the bioassay.
2011-02-17 | E-GEOD-27344 | biostudies-arrayexpress
Project description:The early events of virus infection is one of the more poorly understood areas of plant virology and studies on the effect of virus on the host proteome at very early stages of infection are lacking. In the present study, we analysed the proteome on the early stage changes at 15 minutes post inoculation in the tobacco-TMV pathosystem with and without exogenous application of dsRNA p126
2021-05-12 | PXD022517 | Pride
Project description:Background: The 2009 pandemic H1N1 influenza virus emerged in swine and quickly became a major global health threat. In mouse, non-human primate, and swine infection models, the pH1N1 virus efficiently replicates in the lung and induces pro-inflammatory host responses; however, whether similar or different cellular pathways were impacted by pH1N1 virus across independent infection models remains to be further defined. To address this, we have performed a comparative transcriptomic analysis of acute host responses to a single pH1N1 influenza virus, A/California/04/2009 (CA04), in the lung of mice, macaques and swine. Results: Despite similarities in the clinical course, we observed differences in inflammatory molecules elicited, and the kinetics of their gene expression changes across all three species. The retinoid X receptor (RXR) signaling pathway controlling pro-inflammatory and metabolic processes was differentially regulated during infection in each species, though the heterodimeric RXR partner, pathway associated signaling molecules, and gene expression patterns differed in each species. Conclusions: By comparing transcriptional changes in the context of clinical and virological measures, we identified differences in the host transcriptional response to pH1N1 virus across independent models of acute infection. Antiviral resistance and the emergence of new influenza viruses have placed more focus on developing drugs that target the immune system. Underlying overt clinical disease are molecular events that suggest therapeutic targets identified in one host may not be appropriate in another. The goal of this experiment was to use global gene expression profiling to understand non-human primate lung cellular responses to pandemic H1N1 influenza A/California/04/2009 virus infection. Four-to-fifteen-year-old cynomologous macaques were infected with CA04 virus (n = 4) under anesthesia through a combination of intratracheal (4 ml), intranasal (0.5 ml per nostril), conjunctival (0.5 ml per eyelid) and oral (1 ml) routes with a suspension containing 10^6 TCID50/ml (total infectious dose was 7x10^6 TCID50). Animals were euthanized on 1 and 6 days post-inoculation (n = 2 per time point), and total RNA was extracted from lung samples and analyzed by microarray. Pooled RNA from lungs of uninfected animals served as the reference.
2012-08-13 | E-GEOD-40088 | biostudies-arrayexpress
Project description:RNA interference (RNAi) functions as the major host antiviral defense in insects, while less is understood about how to utilize antiviral RNAi in controlling viral infection in insects. Enoxacin belongs to the family of synthetic antibacterial compounds based on a fluoroquinolone skeleton that has been previously found to enhance RNAi in mammalian cells. In this study, we showed that enoxacin efficiently inhibited viral replication of Drosophila C virus (DCV) and Cricket paralysis virus (CrPV) in cultured Drosophila cells. Enoxacin promoted the loading of Dicer-2-processed virus-derived siRNA into the RNA-induced silencing complex, thereby enhancing antiviral RNAi response in infected cells. Moreover, enoxacin treatment elicited an RNAi-dependent in vivo protective efficacy against DCV or CrPV challenge in adult fruit flies. In addition, enoxacin also inhibited replication of flaviviruses, including Dengue virus and Zika virus, in Aedes mosquito cells in an RNAi-dependent manner. Together, our findings demonstrated that enoxacin can enhance RNAi in insects, and enhancing RNAi by enoxacin is an effective antiviral strategy against diverse viruses in insects, which may be exploited as a broad-spectrum antiviral agent to control vector transmission of arboviruses or viral diseases in insect farming.
2021-11-22 | GSE189204 | GEO
Project description:The goal of the study was to test whether CBD103 genotype of North American gray wolves impacts the gene expression response to polyI:C or to live canine distemper virus. We established 24 primary cultures of epidermal keratinocytes from skin punches of North American gray wolves, and also generated an immortalized keratinocyte line and a CRISPR/Cas9 edited cell line. We evaluated the gene expression response of cells to either 24 hours challenge with 1 ug/ml polyI:C or to five days challenge with live canine distemper virus (100 TCID50/ml). Every challenged cell culture had a paired null control sample (plated and collected at same time points).
2021-05-06 | GSE163163 | GEO