Transcriptomic Analysis of the Intracellular Pathogen Response (IPR)
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE118400 | GEO | 2019/01/08
REPOSITORIES: GEO
Similar Datasets
Project description:We used RNA-seq to identify gene expression changes in C. elegans pals-22 mutants, pals-22 pals-25 double mutants, and pals-25 mutants
2022-09-02 | GSE212552 | GEO
Project description:Intracellular pathogen infection leads to proteotoxic stress in host organisms. Previously we described a physiological program in the nematode C. elegans called the Intracellular Pathogen Response (IPR), which promotes resistance to proteotoxic stress and appears to be distinct from canonical proteostasis pathways. The IPR is controlled by PALS-22 and PALS-25, proteins of unknown biochemical function, which regulate expression of genes induced by natural intracellular pathogens. We previously showed that PALS-22 and PALS-25 regulate the mRNA expression of the predicted ubiquitin ligase component cullin cul-6, which promotes thermotolerance in pals-22 mutants. However, it was unclear whether CUL-6 acted alone, or together with other cullin-ring ubiquitin ligase components, which comprise a greatly expanded gene family in C. elegans. Here we use co-immunoprecipitation studies paired with genetic analysis to define the cullin-RING ligase components that act together with CUL-6 to promote thermotolerance. First, we identify a previously uncharacterized RING domain protein in the TRIM family we named RCS-1, which acts as a core component with CUL-6 to promote thermotolerance. Next, we show that the Skp-related proteins SKR-3, SKR-4 and SKR-5 act redundantly to promote thermotolerance with CUL-6. Finally, we screened F-box proteins that co-immunoprecipitate with CUL-6 and find that FBXA-158 and FBXA-75 promote thermotolerance. In summary, we have defined the three core components and two F-box adaptors of a cullin-RING ligase complex that promotes thermotolerance as part of the IPR in C. elegans, which adds to our understanding of how organisms cope with proteotoxic stress.
2020-02-07 | MSV000084936 | MassIVE
Project description:The immune system continually battles against pathogen-induced pressures, which often leads to the evolutionary expansion of immune gene families in a species-specific manner. For example, the pals gene family expanded to 39 members in the Caenorhabditis elegans genome, in comparison to a single mammalian pals ortholog. Our previous studies have revealed that two members of this family, pals-22 and pals-25, act as antagonistic paralogs to control the Intracellular Pathogen Response (IPR). The IPR is a protective transcriptional response, which is activated upon infection by two molecularly distinct natural intracellular pathogens of C. elegans – the Orsay virus and the fungus Nematocida parisii from the microsporidia phylum. In this study, we identify a previously uncharacterized member of the pals family, pals-17, as a newly described negative regulator of the IPR. pals-17 mutants show constitutive upregulation of IPR gene expression, increased immunity against intracellular pathogens, as well as impaired development and reproduction. We also find that two other previously uncharacterized pals genes, pals-20 and pals-16, are positive regulators of the IPR, acting downstream of pals-17. These positive regulators reverse the effects caused by the loss of pals-17 on IPR gene expression, immunity and development. We show that the negative IPR regulator protein PALS-17 and the positive IPR regulator protein PALS-20 colocalize inside intestinal epithelial cells, which are the sites of infection for IPR-inducing pathogens. In summary, our study demonstrates that several pals genes from the expanded pals gene family act as ON/OFF switch modules to regulate a balance between organismal development and immunity against natural intracellular pathogens in C. elegans.
2023-04-28 | GSE229164 | GEO
Project description:The immune system continually battles against pathogen-induced pressures, which often leads to the evolutionary expansion of immune gene families in a species-specific manner. For example, the pals gene family expanded to 39 members in the Caenorhabditis elegans genome, in comparison to a single mammalian pals ortholog. Our previous studies have revealed that two members of this family, pals-22 and pals-25, act as antagonistic paralogs to control the Intracellular Pathogen Response (IPR). The IPR is a protective transcriptional response, which is activated upon infection by two molecularly distinct natural intracellular pathogens of C. elegans – the Orsay virus and the fungus Nematocida parisii from the microsporidia phylum. In this study, we identify a previously uncharacterized member of the pals family, pals-17, as a newly described negative regulator of the IPR. pals-17 mutants show constitutive upregulation of IPR gene expression, increased immunity against intracellular pathogens, as well as impaired development and reproduction. We also find that two other previously uncharacterized pals genes, pals-20 and pals-16, are positive regulators of the IPR, acting downstream of pals-17. These positive regulators reverse the effects caused by the loss of pals-17 on IPR gene expression, immunity and development. We show that the negative IPR regulator protein PALS-17 and the positive IPR regulator protein PALS-20 colocalize inside intestinal epithelial cells, which are the sites of infection for IPR-inducing pathogens. In summary, our study demonstrates that several pals genes from the expanded pals gene family act as ON/OFF switch modules to regulate a balance between organismal development and immunity against natural intracellular pathogens in C. elegans.
2023-04-28 | GSE229142 | GEO
Project description:We used RNA-seq to identify gene expression changes in C. elegans pals-25(icb98gf) mutants
2022-09-02 | GSE206756 | GEO
Project description:Purpose: To gain molecular insights on how UNC-25 regulates C. elegans innate immunity, we used RNA sequencing to profile gene expression in unc-25(e156) animals relative to wild-type animals with or without P. aeruginosa (PA14) infection. Methods: Synchronized L1 worms were placed onto NGM plates seeded with E. coli OP50 and grown at 20 °C until the L4 stage. Worms were washed off the plates, collected with M9 solution and subsequently transferred to modified NGM plates containing E. coli OP50 or P. aeruginosa PA14 for 24 h at 25 °C. Then, the animals were washed off the plates with M9 solution and frozen in TRIzol (Transgen, ER501-01, China) with liquid nitrogen. Total RNA was isolated using a TransZol Up Plus RNA kit (Transgen, ER501-01, China). Results: RNA seq analyses shows enriched and signficant changed immune genes, neuropeptides, transcription factors and pathways that are dependent of GABA signaling. Conclusion: Our studies uncover that GABA signaling enhance the resistence to pathogen induced killing.
2023-06-26 | GSE195835 | GEO
Project description:Comparison of gene expression in wild-type and zip-1(jy13) mutant animals following bortezomib or DMSO (control) treatment. We report that induction of some genes upon bortezomib treatment is zip-1 dependent.
2021-09-05 | GSE183361 | GEO
Project description:To gain molecular insights on how NMUR-1 regulates C. elegans defense against pathogen infection, we used RNA-Seq to profile gene expression in nmur-1(ok1387) animals relative to wild-type animals with or without E. faecalis or S. enterica infection. We found that NMUR-1 modulates C. elegans transcription activity by regulating the expression of transcription factors, which, in turn, controls the expression of distinct immune genes in response to different pathogens.
2022-02-28 | GSE154324 | GEO
Project description:To gain molecular insights on how UNC-49 regulates C. elegans innate immunity, we used RNA sequencing to profile gene expression in unc-49(e407) animals relative to wild-type animals with or without P. aeruginosa(PA14) infection. We found that UNC-49 suppresses the expression of insulin pathway genes, and lack of UNC-49-mediated suppression in unc-49(e407) animals contributes to their improved survival against P. aeruginosa infection.
2023-10-23 | GSE146406 | GEO
Project description:To understand the molecular mechanism of C. elegans innate immunity, we used RNA sequencing to profile gene expression in wild-type animals with or without P. aeruginosa (PA14) infection. We found that a bZIP transcription factor ZIP-11 is dramatically induced in wild-type worm upon PA14 infection. And ZIP-11 promotes innate immunity through activating PMK-1/p38 pathway and interacting with a CCAAT/enhancer-binding protein CEBP-2.
2022-12-15 | GSE155868 | GEO