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AhR mutant vs N2 wild-type C.elegans, in L1 larval stage

ABSTRACT: Expression profiles of AhR mutant vs N2 wild-type C.elegans, in L1 larval stage compared by using 23232 feature WUSTL microarray

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE16036 | GEO | 2009/12/19

SECONDARY ACCESSION(S): PRJNA115397

REPOSITORIES: GEO

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AhR mutant vs N2 wild-type C.elegans, in L1 larval stage

Project description:Expression profiles of AhR mutant vs N2 wild-type C.elegans, in L1 larval stage compared by using 23232 feature WUSTL microarray 4 ahr-mutant worm samples compared to 3 wild-type samples. Total RNAs purified and reverse transcribed to cDNA and labeled with Cy3-dUTP, and then hybridized on microarray.

2010-05-16 | E-GEOD-16036 | biostudies-arrayexpress

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Identification of Transcription Factor N2::POL II Binding Regions in L1

Project description:modENCODE_submission_2437 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: N2(genotype : wild type genotype : DR subclone of DB original (Tc1 pattern I) official name : N2 ); Developmental Stage: fed L1; Genotype: wild type; Sex: Hermaphrodite; EXPERIMENTAL FACTORS: Developmental Stage fed L1; Target gene ama-1; Strain N2(genotype : wild type genotype : DR subclone of DB original (Tc1 pattern I) official name : N2 ); temp (temperature) 20 degree celsius Series_type: CHIP-seq

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Project description:While immunotherapy has shown efficacy in non-small cell lung cancer (NSCLC) patients, many respond only partially or not at all. One limitation in improving outcomes is the lack of a complete understanding of factors regulating immune checkpoint targets. Here, we sought to address a possible link between an environmental chemical receptor implicated in NSCLC and immune regulation, the aryl hydrocarbon receptor (AhR), and a known but counterintuitive mediator of immunosuppression, IFN , in regulation of two immune checkpoints, PD-L1 and the IDO1, in lung adenocarcinoma (LUAD). To this end we used AhR, PD-L1, and IFN R gene-edited LUAD cell lines, a syngeneic LUAD mouse model, bulk- and single cell-RNA sequencing of LUADs and tumor-infiltrating leukocytes, and existing human transcriptomic databases. The data demonstrate that: 1) the AhR regulates both PD-L1 and IDO1 in murine and human LUAD cells, 2) AhR-driven IDO1 results in production of Kyn which likely mediates an AhR→IDO1→Kyn→AhR amplification loop, 3) the previously characterized induction by IFN of PD-L1 and IDO is mediated by the AhR, 4) transplantation of LUAD cells in which the AhR is deleted results in long-term tumor immunity in approximately half of the mice; slow growing tumors in the other half exhibit significantly higher densities of CD4+ and CD8+ T cells expressing immunocompetence markers, and 5) deletion of either IFN R1 or PD-L1 does not provide the same level of immune protection as AhR deletion. The data definitively link IFN - mediated immunosuppression to the AhR and support the targeting of the AhR in the context of LUAD.

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