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RNA Immunoprecipitation in macrophages using NLRC4 and Caspase11 and high-throughput sequencing of isolated lncRNA

ABSTRACT: RNA Immunoprecipitation in macrophages using NLRC4 and Caspase11 and high-throughput sequencing of isolated lncRNA

PROVIDER: PRJNA725431 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14333202_1.fastq.gz	Fastqsanger.gz
	SRR14333202_2.fastq.gz	Fastqsanger.gz
	SRR14333203_1.fastq.gz	Fastqsanger.gz
	SRR14333203_2.fastq.gz	Fastqsanger.gz
	SRR14333204_1.fastq.gz	Fastqsanger.gz

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RNA Immunoprecipitation in macrophages using NLRC4 and Caspase11 and high-throughput sequencing of isolated lncRNA

Project description:At the epigenetic level, lncRNAs play important roles in cell differentiation and function. We identified novel long-stranded non-coding RNA (GM1082) in BMDMs, which may play an important role in macrophage differentiation and function.To confirm the interaction between LNCRNA and NLRC4 and Caspase11, we performed RNA immunoprecipitation using NLRC4 and Caspase11 antibodies, and high-throughput sequencing of the obtained RNA.

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NLRC4 activation needs lncRNA LNCGM1082

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High Throughput sequencing of NLRC4-T337S/T337S and WT mouse duodenal epithelium

Project description:Purpose: Nlrc4-T337S mice have shown phenotypic differences in their intenstinal epithelia. The goal of this experiment was to determine the differences at the level of transcription between Nlrc4-T337S mice and WT in order to identify further areas of inquiry. Methods: Pooled cDNA libraries were sequenced on Illumina HiSeq 2000 platform, mapped to mm9 using Tophat v2.1, and quantified using Partek GSv6.6 software. Reads were converted to TPM and a 0.5 TPM offset added to all transcripts. Non-coding genes and genes with no sample > 1 TPM were removed Results: Using tophat/2.1.0, we mapped about 50 million sequence reads per sample to the mouse genome (build mm9) and identified 22986 transcripts in the intestines of WT and Nlrc4-T337S mice. Compared to WT IECs, Nlrc4-T337S had a 17-fold increase in Ubd, as well as increases in multiple genes that were identified as part of the MHC-II antigen presentation pathway. Conclusions: Our study found that Nlrc4-T337S IECs have a different RNA-profile than WT mice caused by their point mutation, which led to the discovery of increased proliferation of Nlrc4-T337S IECs as well as increased MHC-II expression.

2018-01-11 | GSE109032 | GEO

Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges

Project description:Bacterial flagellin is a dominant innate immune activator of the intestine. Therefore, we examined the role of the intracellular flagellin receptor, NLRC4, in protecting the gut and/or driving inflammation. In accord with NLRC4 acting via transcription-independent pathways, loss of NLRC4 did not reduce the rapid robust changes in intestinal gene expression induced by flagellin administration. Loss of NLRC4 did not alter basal intestinal homeostasis nor predispose mice to development of colitis upon administration of an anti-IL-10R monoclonal antibody. However, in response to epithelial injury induced by dextran sulfate sodium (DSS), loss of NLRC4 resulted in more severe disease indicating a role for NLRC4 in protecting the gut. Moreover, loss of NLRC4 resulted in increased mortality in response to flagellate, but not aflagellate Salmonella infection. Thus, despite not being involved in rapid intestinal gene remodeling upon detection of flagellin, NLRC4-mediated inflammasome activation protects mice from mucosal and systemic challenges Flagellin (FliC) from WT Salmonella enterica serovar Typhimurium (SL3201, fljB–) was purified through sequential cation and anion-exchange chromatography and purity was verified as previously described 4. WT, T5KO, N4KO and T5/N4-DKO mice (n=6) were given either 0.2 mL PBS or flagellin (10μg/mouse in 0.2 mL PBS) intraperitoneally. After 1h, mice were euthanized and colon was taken and stored in RNAlater (Invitrogen) for 1 day. Total mRNA was isolated from colonic tissues using TRIzol (Invitrogen) and purified using the RNeasy® Plus Mini kit (Qiagen) according to the manufacturer’s instructions

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Cytosolic flagellin receptor NLRC4 protects mice against mucosal and systemic challenges

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SINE RNAs trigger noncanonical NLRC4 inflammasome via DDX17

Project description:Short interspersed element (SINE) RNAs are upregulated by cellular stresses1 (heat shock, DNA damage and viral infection) and accumulate in human diseases (macular degeneration2, lupus3, and Alzheimer’s disease4). These transcripts activate inflammasomes5, a family of cytoplasmic multiprotein complexes that sense danger molecules and initiate innate immune responses by activating caspase-1-dependent cytokine production and inflammatory death6, but the molecular sensor of SINE RNAs is unknown. Here, we identify DDX17, a member of the DEAD box family of RNA helicases7, as a sensor of SINE RNAs requisite for inflammasome activation. Induction of caspase-1 cleavage and release of IL-1 and IL-18 by SINE RNAs requires dual recruitment of NLRP3 and NLRC4 but proceeds independent of NAIPs, immune sensors required for canonical NLRC4 activation by bacterial proteins8,9. Instead, SINE RNAs trigger DDX17–NLRC4 interaction, which licenses inflammasome activation. We also report increased levels of DDX17 protein and association of DDX17 and NLRC4 in the retinal pigmented epithelium (RPE) of human eyes with an advanced, untreatable form of age-related macular degeneration (AMD). Disrupting DDX17–NLRC4 signalling blocks SINE RNA-induced inflammasome activation in human RPE cells and RPE degeneration in an animal model of AMD. Our findings uncover a non-canonical mode of inflammasome activation by endogenous retrotransposon transcripts, and provide new potential targets for macular degeneration and potentially other diseases.

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