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The Toll signaling pathway targets the insulin-like peptide Dilp6 to inhibit growth in Drosophila

ABSTRACT: To identify genes that mediate altered communication between fat body and peripheral tissues, we report the gene expression changes in Drosophila third instar larval fat bodies with or without constitutively-active Toll (Toll10b) to activate innate immune signaling, myristoylated Akt (myrAkt) to activate insulin signaling, or both transgenes to bypass the block from Toll signaling to the upstream part of the insulin signaling pathway

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE133662 | GEO | 2019/07/02

REPOSITORIES: GEO

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Formation of polarized contractile interfaces by self-organized Toll-8/Cirl GPCR asymmetry

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

The Toll signaling pathway targets the insulin-like peptide Dilp6 to inhibit growth in Drosophila

Project description:The Toll signaling pathway targets the insulin-like peptide Dilp6 to inhibit growth in Drosophila

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Identification of Toll-like receptor 4 interacting partner through immunoprecipitation-based chemical cross-linking proteomics

Project description:Toll-like receptor 4 (TLR-4) is a transmembrane protein. Its activation leads to NF-kB signaling pathway and proinflammatory cytokines’ production that are responsible for activating innate immunity system. Here, we design a co-immunoprecipitation based cross-linking proteomics approach to reveal the TLR-4 interactome upon treatment of lipopolysaccharides and statin drug in HA-TLR-4 transfected HEK293 cells. A total of 712 differentially expressed proteins were identified and quantified in this study. Selected candidate proteins, macrophage myristoylated alanine-rich C kinase substrate, and creatine kinase, exclusively identified in the treatment of statin along with cross-linkers, were further validated by immunoblotting.

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Toll-like receptors 2 and 4 control adaptive β-cell expansion in diet-induced obesity

Project description:Adult pancreatic β cells are refractory to proliferation, a roadblock for the treatment of insulin-deficient diabetes. Consumption of energy-dense Western or high-fat diet (HFD) triggers mild adaptive β cell mass expansion to compensate for peripheral insulin resistance; however, the underlying molecular mechanism remains unclear. Here we show that Toll-like receptors (TLR) 2/TLR4 act as molecular “brakes” for diet-induced β cell replication in both mice and humans. The combined loss of TLR2/TLR4, but not individually, dramatically increases facultative β, not α, cell replication, leading to progressively enlarged islet mass and hyperinsulinemia in diet-induced obesity. Mechanistically, loss of TLR2/TLR4 increases β cell proliferation and nuclear abundance of Cyclin D2 and CDK4 in an extracellular signal-regulated kinase (ERK)-dependent manner. These data reveal a novel mechanism governing adaptive β cell mass expansion in diet-induced obesity and suggest that selective targeting of TLR2/TLR4 pathways may hold promise for reversing β cell failure in diabetic patients.

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Luteolin attenuates hepatic and adipocyte fibrosis and insulin resistance by targeting toll-like receptors signaling pathway in diet-induced obese mice

Project description:The flavonoid luteolin possess a variety of anti-inflammatory properties, but little has known about the detailed mechanisms linked to the anti-metabolic syndrome action of luteolin based on the integration of the transcriptional profile and the phenotype biomarkers. The aim of this study was to investigate the protective role of luteolin on inflammation-mediated metabolic diseases, focusing on its role in modulating toll-like receptor (TLR) signaling pathway triggered up-regulation of pro-inflammatory cytokines. Above all, it provides novel insights into the effect of luteolin on the link among adiposopathy, insulin resistance, hepatic steatosis and fibrosis. C57BL/6J mice were fed a normal, high-fat, and high-fat + 0.005% (w/w) luteolin diet for 16 weeks. In this study, (a) luteolin treatment resulted in an improvement in chronic low-grade inflammation by modulating TLR-signaling pathway resulting in reduced pro-inflammatory cytokines and macrophage accumulation; (b) there is a positive relationship of TLR5, MKK4/7, p38 and JNK-related gene expressions and lipogenesis in luteolin-treated obese mice, which is linked to an attenuation of hepatic lipotoxicity with an increased hepatic anti-oxidant system; (c) luteolin prevented hepatic and adipocyte fibrosis by decreasing ECM accumulation and cathepsin gene expressions; (d) Emr1 and Ccl7 genes, important markers inducing low-grade inflammation, are affected by advancing age as well as body weight, and luteolin treatment normalized those gene expressions; (e) luteolin treatment improved insulin resistance by normalizing pancreatic islet dysfunction, and differentially modulating the plasma GLP-1 and GIP levels. Taken together, luteolin ameliorates the deleterious effects of diet-induced obesity and its comorbidity.

2018-03-06 | GSE111412 | GEO

Drosophila lncRNA-NANPI enhances Toll signaling pathway by interacting with Dif/Dorsal to facilitate transcription of antibacterial peptides

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.

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Gene expression analysis in the aorta from non-diabetic or STZ-induced diabetic apolipoprotein E deficient (ApoE-/-) mice fed with high fat diet in the presence or absence of PKC Î² inhibitor, ruboxistaurin (RBX, or LY333531)

Project description:We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C-Î² isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling. To further investigate the effect of high fat diet and specific PKC Î² inactivation on STZ-induced atherosclerosis using the PKC Î² inhibitor, ruboxistaurin (RBX, or LY333531), ApoE-/- mice were used and fed with high fat diet (42% of fat Kcal) with or without RBX after onset of diabetes. Isolated total RNA from whole aortas of each group was used and analyzed for gene expression. The gene expression profiles were processed by using the Microarray Suite version 5.0 (MAS 5.0) with Affymetrix default analysis settings. ApoE-/- mice were used as a rodent atherosclerosis model. Isolated total RNA from aortas of each ApoE-/- mouse fed with high fat diet for 10 weeks after STZ-induced diabetes or control groups were used for preparation and hybridization on Affymetrix microarrays. There were total 4 different mice groups, which were fed with high fat diet with or without RBX. Each group had four individual mouse (N=4).

2016-03-26 | E-GEOD-79623 | biostudies-arrayexpress

Project description:We found that hyperglycemia and elevated fatty acids in diabetes could activate protein kinase C-β isoforms and selectively induce insulin resistance via inhibiting vascular insulin signaling. To further investigate the effect of high fat diet and specific PKC β inactivation on STZ-induced atherosclerosis using the PKC β inhibitor, ruboxistaurin (RBX, or LY333531), ApoE-/- mice were used and fed with high fat diet (42% of fat Kcal) with or without RBX after onset of diabetes. Isolated total RNA from whole aortas of each group was used and analyzed for gene expression. The gene expression profiles were processed by using the Microarray Suite version 5.0 (MAS 5.0) with Affymetrix default analysis settings.

2016-03-26 | GSE79623 | GEO

Effect of Endogenous Stimuli-Responsive Separating Microneedles to Inhibit Hypertrophic Scar on Rabbit Ear

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