Analysis of gene expression changes upon infection of C.elegans with Orsay virus
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE41056 | GEO | 2013/06/01
SECONDARY ACCESSION(S): PRJNA175638
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of the transcriptional response to viral infection in C.elegans. Comparison of infected and uninfected animals for three strains: N2 (resistant), JU1580 (sensitive), RDE-1 (sensitive)
2013-06-01 | E-GEOD-41056 | biostudies-arrayexpress
Project description:Attempt to identify small non-coding RNAs that change in levels as a result of viral infection of C.elegans
2013-06-01 | GSE41057 | GEO
Project description:Attempt to identify small non-coding RNAs that change in levels as a result of viral infection of C.elegans Small non-coding RNA (18-30nt) was extracted from animals either infected with Orsay virus or uninfected as indicated.
2013-06-01 | E-GEOD-41057 | biostudies-arrayexpress
Project description:Across metazoans, innate immunity is vital in defending organisms against viral infection. In mammals, antiviral innate immunity is orchestrated by interferon signaling, activating the STAT transcription factors downstream of the JAK kinases to induce expression of antiviral effector genes. In the nematode C. elegans, which lacks the interferon system, the major antiviral response so far described is RNA interference but whether additional gene expression responses are employed is not known. Here we show that, despite the absence of both interferon and JAK, the C. elegans STAT homologue STA-1 orchestrates antiviral immunity. Intriguingly, mutants lacking STA-1 show increased resistance to antiviral infection. Using gene expression analysis and chromatin immunoprecipitation we show that, in contrast to the mammalian pathway, STA-1 acts as a transcriptional repressor. Thus STA-1 might act to suppress a constitutive antiviral response in the absence of infection. Using a reverse genetic screen we identify the SID-3 as a kinase upstream of STA-1 in the response to infection. Together, our work identifies a novel STAT regulatory cascade controlling its activity in antiviral resistance, illustrating the complex evolutionary trajectory displayed by innate immune signaling pathways across metazoan organisms.
2017-08-11 | GSE95228 | GEO
Project description:Across metazoans, innate immunity is vital in defending organisms against viral infection. In mammals, antiviral innate immunity is orchestrated by interferon signaling, activating the STAT transcription factors downstream of the JAK kinases to induce expression of antiviral effector genes. In the nematode C. elegans, which lacks the interferon system, the major antiviral response so far described is RNA interference but whether additional gene expression responses are employed is not known. Here we show that, despite the absence of both interferon and JAK, the C. elegans STAT homologue STA-1 orchestrates antiviral immunity. Intriguingly, mutants lacking STA-1 show increased resistance to antiviral infection. Using gene expression analysis and chromatin immunoprecipitation we show that, in contrast to the mammalian pathway, STA-1 acts as a transcriptional repressor. Thus STA-1 might act to suppress a constitutive antiviral response in the absence of infection. Using a reverse genetic screen we identify the SID-3 as a kinase upstream of STA-1 in the response to infection. Together, our work identifies a novel STAT regulatory cascade controlling its activity in antiviral resistance, illustrating the complex evolutionary trajectory displayed by innate immune signaling pathways across metazoan organisms.
2017-08-11 | GSE95229 | GEO
Project description:This experiment investigates the gene expression differences upon Orsay virus infection in the Caenorhabdits elegans strains N2 and CB4856. Assays measuring viral load found that the N2 strain displays higher viral loads upon infection than the CB4856 strain. The goal of the experiment was to identify gene-expression differences that could explain the differences in viral load. We (mock-)infected 26h-old C. elegans populations with Orsay virus and took samples after 30h of infection. For each treatment-strain combination 8 samples were collected. Thereafter RNA was isolated, labelled, and hybridized on microarray.
2020-07-08 | E-MTAB-7574 | biostudies-arrayexpress
Project description:We discovered 5446 genes expression change (4218 genes from P0 to F2) in wild-type C.elegans transcriptome compared to DAMT-1 mutant upon mitochondrial stress by RNA-seq, which indicated those genes response to mitochondrial stress and may function in mitochondrial stress response.
2018-09-27 | GSE118175 | GEO
Project description:We discovered 364 peaks enrichment change in wild-type C.elegans genome by 6mA MeDIP-seq, which indicated those genes response to mitochondrial stress and may function in mitochondrial stress response.
2018-09-27 | GSE118268 | GEO
Project description:Comparison of the proteome and phosphoproteome of wild type C.elegans embryos compared to pig-1 mutant embryos
2017-12-11 | PXD005752 | Pride
Project description:The same entry pathway is shared by HBV and HDV. Both viruses attach to hepatocytes via heparansulfate proteoglycan and utilize sodium taurocholate co-transporting polypeptide (NTCP) for a specifc entry. This specific entry step is inhibited by Myrcludex B, a 47-aa lipopeptide myristoylated at the N-terminus. Here we compared the cellular response in the gene expression level triggerred by both viruses. The microarray data shows that HBV infection leads to a silent response but HDV infection triggers high level of innate response such as inteferon-stimulated genes (ISG) expression. Moreover, the response depends on the hepatic cell lines used for infection. Compared to HepG2 cells, HuH7 can not induce ISG even infected by HDV. Abstract of manuscript: Background & aims: Hepatitis B virus (HBV) and D virus (HDV) co-infections cause the most severe form of viral hepatitis. HDV induces an innate immune response, but it is unknown how the host cell senses HDV and if this defense affects HDV replication. We aim to characterize interferon (IFN) activation by HDV, identify the responsible sensor and evaluate the effect of IFN on HDV replication. Methods: HDV and HBV susceptible hepatoma cell lines and primary human hepatocytes (PHH) were used for infection studies. Viral markers and cellular gene expression were analyzed at different time points after infection. Pattern recognition receptors (PRRs) required for HDV-mediated IFN activation and the impact on HDV replication were studied using stable knock-down or overexpression of the PRRs. Results: Microarray analysis revealed that HDV but not HBV infection activated a broad range of interferon stimulated genes (ISGs) in HepG2NTCP cells. HDV strongly activated IFN-β and IFN-λ in cell lines and PHH. HDV induced IFN levels remained unaltered upon RIG-I or TLR3 knock-down, but were almost completely abolished upon MDA5 depletion. Conversely, overexpression of MDA5 but not RIG-I and TLR3 in Huh7.5NTCP cells partially restored ISG induction. During long-term infection, IFN levels gradually diminished in both HepG2NTCP and HepaRGNTCP cell lines. MDA5 depletion had little effect on HDV replication despite dampening HDV-induced IFN response. Moreover, treatment with type I or type III IFNs did not abolish HDV replication. Conclusions: Active replication of HDV induces an IFN-β/λ response, which is predominantly mediated by MDA5. This IFN response and exogenous IFN treatment have only a moderate effect on HDV replication in vitro indicating the adaption of HDV replication to an IFN activated state.
2018-01-30 | GSE109824 | GEO