Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of Dorsal, Dif, and Relish mutation on Drosophila response to G- Bacteria

ABSTRACT: The abstract of the manuscript titled "Microarray analyses reveal possible new targets for the Rel protein Dif in Drosophila melanogaster " is given below: The fruit fly Drosophila melanogaster express three closely related NF-κB-like transcription factors: Dorsal, Dif, and Relish. They share significant sequence identity in their DNA binding Rel homology domain and bind similar DNA sequence motifs. These factors play an important role in the transcription of Drosophila humoral immune proteins such as antimicrobial peptides during infection. To study their roles in vivo, we used microarrays to determine the effect of null mutations in individual Rel transcription factors on larval gene expression. Of the 188 genes that were significantly upregulated in wildtype larvae upon bacterial challenge, overlapping but distinct groups of genes were affected in the Rel mutants. We also ectopically expressed Dorsal or Dif and used cDNA microarrays to determine the genes that were up-regulated in the presence of these transcription factors. Combining this data, we identified novel genes that may be specific targets of Dif. Keywords: genetic modification

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE5489 | GEO | 2007/04/16

SECONDARY ACCESSION(S): PRJNA96127

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of Drosophila mutant for transcription factors Dorsal, Dif, and Relish and their effect on immune response

Project description:The abstract of the manuscript titled "Microarray analyses reveal possible new targets for the Rel protein Dif in Drosophila melanogaster " is given below: ; The fruit fly Drosophila melanogaster express three closely related NF-ÎºB-like transcription factors: Dorsal, Dif, and Relish. They share significant sequence identity in their DNA binding Rel homology domain and bind similar DNA sequence motifs. These factors play an important role in the transcription of Drosophila humoral immune proteins such as antimicrobial peptides during infection. To study their roles in vivo, we used microarrays to determine the effect of null mutations in individual Rel transcription factors on larval gene expression. Of the 188 genes that were significantly upregulated in wildtype larvae upon bacterial challenge, overlapping but distinct groups of genes were affected in the Rel mutants. We also ectopically expressed Dorsal or Dif and used cDNA microarrays to determine the genes that were up-regulated in the presence of these transcription factors. Combining this data, we identified novel genes that may be specific targets of Dif. Experiment Overall Design: This study uses Affymetrix chips to study the effect on gene expression when third instar larvae are injected with PBS or E. coli bacteria. Wildtype, Dorsal1 mutant, Dif1 mutant, and Relish E20 mutant larvae are used to determine the effect of the mutations on gene expression.

2008-06-13 | E-GEOD-5489 | biostudies-arrayexpress

The effect of ectopic expression of Dorsal and Dif on Drosophila Gene Expression

Project description:This study explores the effect of ectopic expression of Dorsal and Dif on Drosophila larval gene expression. The abstract of the manuscript we are submitting follows: Microarray analyses reveal possible new targets for the Rel protein Dif in Drosophila melanogaster The fruit fly Drosophila melanogaster express three closely related NF-κB-like transcription factors: Dorsal, Dif, and Relish. They share significant sequence identity in their DNA binding Rel homology domain and bind similar DNA sequence motifs. These factors play an important role in the transcription of Drosophila humoral immune proteins such as antimicrobial peptides during infection. To study their roles in vivo, we used microarrays to determine the effect of null mutations in individual Rel transcription factors on larval gene expression. Of the 188 genes that were significantly upregulated in wildtype larvae upon bacterial challenge, overlapping but distinct groups of genes were affected in the Rel mutants. We also ectopically expressed Dorsal or Dif and used cDNA microarrays to determine the genes that were up-regulated in the presence of these transcription factors. Combining this data, we identified novel genes that may be specific targets of Dif. Keywords: Genetic Modification

2007-04-16 | GSE5469 | GEO

Heterozygous mutation of NF-B innate immune response transcription factor Relish increases survival following traumatic brain injury in Drosophila

Project description:Traumatic brain injury (TBI) pathologies are caused by primary and secondary injuries. Primary injuries result from physical damage to the brain, and secondary injuries arise from cellular responses to primary injuries. A characteristic cellular response is sustained activation of inflammatory pathways commonly mediated by NF-B transcription factors. Using a Drosophila melanogaster TBI model, we previously found that the main proximal transcriptional response to primary injuries is triggered by activation of Toll and Imd innate immune response pathways that engage NF-B factors Dif and Relish (Rel), respectively. Here, we monitor the abundance of Rel protein by mass spectrometry (MS) and observe that Rel increases in fly heads at 4-8 h after TBI. To investigate the necessity of Rel for secondary injuries, we generated a null allele, Reldel, by CRISPR/Cas9 editing. Heterozygous but not homozygous Reldel mutation reduced mortality at 24 h after TBI and increased the lifespan of injured flies. Additionally, the effect of heterozygous Reldel mutation on mortality was modulated by genetic background and diet. To identify genes that facilitate effects of heterozygous Reldel mutation on TBI outcomes, we compared genome-wide mRNA expression profiles of uninjured and injured +/+, +/Reldel, and Reldel/Reldel flies at 4 h following TBI. Only a few genes changed expression more than two-fold in +/Reldel flies relative to +/+ and Reldel/Reldel flies, and they were not canonical innate immune response genes. Therefore, Rel is necessary for TBI-induced secondary injuries but in complex ways involving Rel gene dose, genetic background, diet, and possibly small changes in expression of innate immune response genes.

2020-12-04 | PXD021869 | Pride

lncRNA-CR11538 functions as a decoy of Dif/Dorsal to negatively regulate Drosophila Toll immune responses

Project description:The maintenance of innate immune homeostasis is critical for animal survival to combat pathogens. Although many positive or negative protein factors have been identified, little is known about the long non-coding RNA that regulates the Toll pathway. Herein, we have discovered a novel lncRNA-CR11538 highly activated during the Drosophila response to gram+ bacterial infection. The transient overexpression of CR11538 inhibited the expression of antimicrobial peptides (Drosomycin and Metchnikowin) in vivo to suppress Toll signaling pathway. Remarkably, core enrichment genes based on RNAseq, subcellular localization and RIP suggest that CR11538 can interact with the transcription factor Dif/Dorsal in nucleus. ChIP-qPCR and dual luciferase report experiments show that CR11538 can sequester Dif/Dorsal away from the promoter thus suppressing the transcription of antimicrobial peptides. In summary, we discovered a novel lncRNA-CR11538 that negatively regulate the Drosophila Toll pathway. It broadens our understanding of the regulatory mechanism of Toll pathway involving lncRNA and provides insights for the research on innate immune system of insects and mammals.

2021-08-13 | GSE181870 | GEO

The effect of osa RNAi with and without infection

Project description:Transcriptome profiling of immune-responsive genes in Drosophila melanogaster during Gram-positive bacterial infection and upon silencing of osa was performed. The most highly induced gene in the control set (150071 Valanne I) by Micrococcus luteus infection was CR44404, and its expression is fully dependent on osa expression (as shown in this dataset, 150071 Valanne II). The full transcriptome analysis also indicated that Osa regulates the expression of immune genes by modifying the expression of the Drosophila NF-kappaB factors Relish and Dif.

2020-02-13 | GSE120443 | GEO

Relish-mediated lncRNA-CR33942 facilitates Drosophila Imd immune responses and promotes antimicrobial peptide expression via interacting with Relish

Project description:Long noncoding RNAs (lncRNAs), as a class of emerging regulators, play crucial role in regulating the strength and duration of innate immunity. However, little is known about how these Drosophila Imd immunity-related lncRNAs are regulated. Herein, we firstly revealed that overexpression of lncRNA-CR33942 could strengthen the expression of Imd pathway antimicrobial peptides Diptericin (Dpt) and Attacin-A (AttA) after infection, and vice versa. Secondly, RNA-seq analysis of post-infected lncRNA-CR33942-overexpressing flies further confirmed that lncRNA-CR33942 positively regulates the Drosophila Imd pathway. Mechanistically, we indicated that lncRNA-CR33942 interacts with NF-κB transcription factor Relish to promote its binding to Dpt and AttA promoters, thereby facilitating Dpt and AttA expression. Interestingly, we found that Relish can also directly promote lncRNA-CR33942 transcription by binding to its promoter. Finally, rescue experiments and dynamic expression profiling post-infection demonstrated the vital role of the Relish/lncRNA-CR33942/AMPs regulatory axis in enhancing inadequate Imd immune responses and maintaining immune homeostasis. Taken together, our study not only elucidates a novel mechanism about lncRNA in Drosophila Imd immune regulation, but also has important guiding significance for elucidating the complex regulatory mechanism of animal innate immune response.

2022-03-22 | GSE198991 | GEO

lncRNA-CR46018 as a positive regulator controls Drosophila Toll immune response by interacting with Dif/Dorsal  

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

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.

2021-05-07 | GSE174007 | GEO

Drosophila melanogaster

Project description:Effect of Dorsal, Dif, and Relish mutation on Drosophila response to G- Bacteria

| PRJNA96127 | ENA

Comparative microarray analysis of psh and Dif mutant flies treated with Metarhizium anisopliae ARSEF 549

Project description:The Toll pathway is the chief antifungal pathway in Drosophila. Two components of this pathway have disparate effects on Drosophila infected with Metarhizium ansiopliae ARSEF 549 (Ma549). Infected Drosophila Dif mutants show no change in susceptibility while infected psh mutants rapidly succumb to infection. We evaluated the impact of Ma549 on gene regulation in flies deficient in these Toll pathway components to identify the cause for these susceptibility differences. Four fly lines were used: psh, BDSC6326 (psh control), Dif, and cn bw (Dif control). RNA was collected 46 hrs post infection for 10 infected or uninfected male flies per replicate.

2022-08-31 | E-MTAB-9527 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data