Onychophoran Toll gene expression
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PROVIDER: PRJEB23025 | ENA |
REPOSITORIES: ENA
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Project description:Tissue morphogenesis requires the spatial control over actomyosin contractility to drive cell shape changes. How developmental patterning information controls cell mechanics is poorly understood. In the Drosophila embryo ectoderm, Myosin-II is enriched at the interface between antero-posterior neighboring cells, leading to planar polarized cell intercalation. G protein-coupled receptors (GPCRs) are required for planar polarized Myosin-II activation at junctions and Toll receptors provide a positional code underlying this process. How Toll receptors polarize actomyosin contractility remains unknown. Here we report that cells expressing different levels of a single Toll receptor Toll-8 activate Myosin-II at their interface. Surprisingly, the Toll-8 intracellular domain is not required for signaling at cell interfaces suggesting signaling by proxy. We found that Toll-8 forms a molecular complex with the adhesion GPCR Cirl/Latrophilin that is required for Toll-8 dependent junctional Myosin-II activation. Strikingly, the interfaces between Cirl expressing and cirl mutant cells also activate Myosin-II suggesting that Toll-8 induces Cirl asymmetric signaling at cell interfaces. We further showed that Toll-8 recruits Cirl both in trans and in cis, inducing asymmetric Cirl localization at the boundary of the Toll-8 expression domain. Finally, we found that Toll-8 and Cirl exhibit dynamic interdependent planar polarization when neighboring cells express different levels of Toll-8. Through this feedback, Toll-8 and Cirl self-organize planar polarized signaling.
2021-04-22 | PXD017895 | Pride
Project description:The aim of this study is to investigate the interaction between diet - primary meat and fiber - and polymorphisms in Toll-like receptors in relation to risk of colorectal cancer in a Danish prospective cohort.
| 2251863 | ecrin-mdr-crc
Project description:Canine heartworm is a widespread and potentially fatal mosquito-borne disease caused by infections with the parasitic nematode, Dirofilaria immitis. We have previously shown that systemic activation of the Toll immune pathway via silencing of the negative regulator Cactus in Aedes aegypti blocks parasite development in the Malpighian tubules, the mosquito renal organ. However, it was not established whether the Malpighian tubules were directly responding to Toll activation or were alternatively responding to upregulated proteins or other changes to the hemolymph driven by other tissues. Distinguishing these possibilities is crucial for developing more precise strategies to block D. immitis while potentially avoiding the fitness cost to the mosquito associated with Cactus silencing. This study defines the transcriptional response of Ae. aegypti Malpighian tubules after systemic Toll activation via intra-thoracic injection of dsCactus and found, like the response of whole mosquitoes, a significant increase in expression of Toll pathway target genes. Additionally, we identified a significant overlap between the transcriptional response of the Malpighian tubules and proteins upregulated in the hemolymph. Our data show that Malpighian tubules are capable of RNAi-mediated gene silencing and directly respond to dsCactus treatment by upregulating canonical Toll pathway targets. Though not definitive, the strong correspondence between the Malpighian tubule transcriptional and the hemolymph proteomic responses provides evidence that the tubules may contribute to mosquito humoral immunity.
2024-08-27 | PXD036225 | Pride
Project description:Toll like receptor 3 (TLR3) is an endosomal pattern recognition receptor (PRR), recognizing double stranded RNA (dsRNA) as a distinct Pathogen-associated molecular pattern (PAMP) for viral infections. We aim to understand the contribution of TLR3 to the dsRNA response in hepatocytes. The innate immune response of cells of hepatic origin (Huh7, Huh7.5, PH5CH and primary human hepatocytes (PHH)) was analyzed by transcriptome analysis (RNAseq) upon supernatant delivery or transfection of synthetic dsRNA (poly(I:C)). Expression of TLR3 and RIG-I was reconstituted by lentiviral transduction in Huh7 and Huh7.5 cells. Huh7 and Huh7.5 cells, devoid of functional TLR3 expression, did not respond to supernatant delivery of poly(I:C), in contrast to PH5CH and PHH, confirming a high selectivity of this method towards activating TLR3 in all hepatocyte models.
| EGAS00001005147 | EGA
Project description:To investigate the similarity of toll-like receptor tolerance in macrophages stimulated with different toll-like receptor ligands we stimulated naïve or tolerant macrophages with ligands for TLR4, TLR2, TLR3 and TLR9. The data identifies a core set of genes that are tolerised by all ligands and genes that show TLR specific patterns.
2018-05-30 | GSE81291 | GEO
Project description:LncRNAs have important regulatory functions but their roles in Drosophila innate immunity are poorly understood. The Drosophila Toll signaling pathway responds to Gram-positive bacterial infection and is highly conserved with mammalian TLR signaling. Recent studies focused mainly on Toll signaling pathway regulation by protein-coding genes. In the present study, we found that lncRNA-CR33942 was upregulated after Micrococcus luteus infection. Gain-of-function and loss-of-function assays disclosed that lncRNA-CR33942 regulates the Toll signaling pathway and affects Drosophila survival. RNA-seq of infected CR33942-overexpressing flies was performed to explore the CR33942 mechanism. About 70% of all upregulated core enrichment genes in the Toll signaling pathway were antibacterial peptides and PGRPs transcribed by Dif/Dorsal. We also demonstrated CR33942 interactions with Dif/Dorsal and revealed that they induce antibacterial peptides. Hence, we renamed CR33942 as lncRNA-NANPI (NF-κB-associated non-coding RNA promotional immunology). The present study identified the novel Toll signaling pathway regulator NANPI, elucidated its mode of action, clarified the function of lncRNA, and expanded our understanding of the Toll signaling pathway.
2021-05-07 | GSE174007 | GEO
Project description:Toll mediates a robust and effective innate immune response across vertebrates and invertebrates. In Drosophila melanogaster, activation of Toll by systemic infection drives the accumulation of a rich repertoire of immune effectors in hemolymph, including the recently characterized Bomanins as well as the classical antimicrobial peptides (AMPs). Here we report the functional characterization of a Toll-induced hemolymph protein encoded by the bombardier (CG18067) gene. Using the CRISPR-Cas9 system to generate a precise deletion, we found that Bombardier is required for Toll-mediated defense against fungi and Gram-positive bacteria. Assaying cell-free hemolymph from these flies, we found that the Bomanin-dependent candidacidal activity observed in hemolymph is also dependent on Bombardier, but not on the antifungal AMPs Drosomycin and Metchnikowin. Using mass spectrometry, we demonstrated that deletion of Bombardier results in the specific absence of short-form Bomanins from hemolymph. Flies lacking Bombardier also exhibited a defect in pathogen tolerance that we trace to an autoimmune disorder triggered by Toll activation. These results lead us to a model in which the presence of Bombardier in wild-type flies enables the proper folding, secretion, or intermolecular associations of short-form Bomanins, and the absence of Bombardier disrupts one or more of these steps, resulting in defects in both immune resistance and tolerance.
2019-10-25 | MSV000084509 | MassIVE
Project description:Toll pathway is a key mediator of antiplasmodial immunity and its mechanism of action is dependent on hemocytes (mosquito white blood cells). Anopheles gambiae were injected with dsRNA for Cactus, an inhibitor of the Toll pathway. Cactus silencing over activates the Toll pathway. The goal of this experiment is to evaluate hemocyte transcriptional changes between control mosquitoes injected with a non-related dsRNA (dsLacZ and dsCactus injected mosquitoes. We also divide hemocytes from control and experimental conditions into 2 groups: bound (hemocytes that attach to glass - granulocyte populations) and unbound (hemocytes that remain in suspension - prohemocytes and oenocytoids). Files from Unbound fractions are labelled: UB and from bound fractions are labelled B. Some of the samples were run twice and have 2 gz files.
2021-12-16 | E-MTAB-11252 | biostudies-arrayexpress
Project description:The Toll signaling pathway is highly conserved from insects to mammals. Drosophila is a model species that is commonly used to study innate immunity. Although many studies have assessed protein-coding genes that regulate the Toll pathway, it is unclear whether long noncoding RNAs (lncRNAs) play regulatory roles in the Toll pathway. Here, we evaluated the expression of the lncRNA CR46018 in Drosophila. Our results showed that this lncRNA was significantly overexpressed after infection of Drosophila with Micrococcus luteus. A CR46018-overexpressing Drosophila strain was then constructed; we expected that CR46018 overexpression would enhance the expression of various antimicrobial peptides downstream of the Toll pathway, regardless of infection with M. luteus. RNA-seq analysis of CR46018-overexpressing Drosophila after infection with M. luteus showed that upregulated genes were mainly enriched in Toll and Imd signaling pathways. Moreover, bioinformatics predictions and RNA-immunoprecipitation experiments showed that CR46018 interacted with the transcription factors Dif and Dorsal to enhance the Toll pathway. During gram-positive bacterial infection, flies overexpressing CR46018 showed favorable survival compared with flies in the control group. Based on these findings, we renamed CR46018 as lncRNA-RDIP. Overall, our current work not only reveals a new immune regulatory factor, lncRNA-RDIP, and explores its potential regulatory model, but also provides a new perspective for the effect of immune disorders on the survival of Drosophila melanogaster.
2021-05-20 | GSE174684 | GEO