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Genome wide screening for binding target of ELF3 transcription factor in biliary epithrial cell line HBDEC2

ABSTRACT: ELF3, a member of E26 transformation-specific transcription factors, is inactivated in a range of cancers including biliary tract cancer. We performed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-Seq) to identify direct ELF3 target genes. The number of uniquely mapped reads identified by ChIP-Seq was 109.9 M for the ELF3 binding site and 59.7 M for the control input DNA. These read data were evaluated with MACS 1.4, and 13,960 peaks were identified throughout the genome with a false discovery rate (FDR) of < 0.1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156165 | GEO | 2020/08/27

REPOSITORIES: GEO

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Expression profiling analysis of an inducible ELF3-expressing and control human bile duct cells [inducible ELF3]

Project description:An immortalized normal epithelial cell line of common bile duct origin (HBDEC2 cells) was established. An inducible ELF3-expressing was generated by infection with the retrovial vector pRetroX-TetOne-Puro-ELF3-flag, expressing ELF3 fused to a flag-tag.

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RNA-Seq and ChIP-Seq profiling of ELF3, an prion-like domain-containig in ELF3 that functions as a thermosensor in Arabidopsis.

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Genome wide screening for binding target of ELF3 transcription factor in biliary epithrial cell line HBDEC2

Project description:Genome wide screening for binding target of ELF3 transcription factor in biliary epithrial cell line HBDEC2

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mRNA expression profiling of ERCP biliary brushings of malignant biliary strictures

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Project description:Plants regulate their time to flowering by gathering information from the environment. Photoperiod and temperature are among the most important environmental variables. Suboptimal, but not near-freezing, temperatures regulate flowering through the thermosensory pathway, which overlaps with the autonomous pathway. Here we show that ambient temperature regulates flowering by two genetically distinguishable pathways, one that requires TFL1 and another that requires ELF3. The delay in flowering time observed at lower temperatures was partially suppressed in single elf3 and tfl1 mutants, whereas double elf3 tfl1 mutants were insensitive to temperature. tfl1 mutations abolished the temperature response in cryptochrome mutants that are deficient in photoperiod perception, but not in phyB mutants that have a constitutive photoperiodic response. Contrary to tfl1, elf3 mutations were able to suppress the temperature response in phyB mutants, but not in cryptochrome mutants. The gene expression profile revealed that the tfl1 and elf3 effects are due to the activation of different sets of genes and identified CCA1 and SOC1/AGL20 as being important cross talk points. Finally, genome-wide gene expression analysis strongly suggests a general and complementary role for ELF3 and TFL1 in temperature signalling. Three genotypes, WT (Columbia), elf3-7 and tfl1-1 mutants. Three biological replicates for each condition (genotype X temperature combination). RNA prepared independently for each sample.

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Expression profiling of isogenic A549 cell lines with and without ELF3 knock-down

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Identification of differentially expressed miRNAs after knockdown of ELF3-AS1 in gastric cancer

Project description:In this study, we used miRNA sequencing to analyze and identify possible miRNAs that can be regulated by and ELF3-AS1 in gastric cancer. The results showed that lncRNA ELF3-AS1 knockdown decreased the expression of miR-33a/b and miR-203a. Due to miR-33a/b and miR-203a were able to target SNAI2 expression, and ELF3-AS1 knockdown significantly upregulates SNAI2 expression, we speculated ELF3-AS1 may negatively regulate SNAI2 expression through positively regulating the expression of miR-33a/b and miR-203a in GC.

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ELF3 activated by a super-enhancer and an autoregulatory feedback loop is required for high level HLA-C expression on extravillous trophoblasts

Project description:HLA-C arose during evolution of pregnancy in the Great Apes 10-15 million years ago. It has a dual function on placental extravillous trophoblasts (EVT) as it contributes to both tolerance and immunity at the maternal-fetal interface. The mode of its regulation is of considerable interest in connection with the biology of pregnancy and pregnancy abnormalities. First trimester primary EVT in which HLA-C is highly expressed, as well as JEG3, an EVT model cell lines, were employed. Single cell RNA-seq data and quantitative PCR identified high expression of the transcription factor ELF3 in those cells. ChIP-PCR confirmed that both ELF3 and MED1 bound to the proximal HLA-C promoter region. However, binding of RFX5 to this region was absent or severely reduced and the adjacent HLA-B locus remained closed. Expression of HLA-C was inhibited by ELF3 siRNAs and by wrenchnolol treatment. Wrenchnolol is a cell-permeable synthetic organic molecule that mimics ELF3 and is relatively specific for binding to ELF3’s coactivator, MED23, as our data also showed in JEG3. Moreover, the ELF3 gene is regulated by a super-enhancer that spans more than 5 Mb, identified by ATAC-seq, as well as by its sensitivity to (+)-JQ1 (inhibitor of BRD4). ELF3 bound to its own promoter, thus creating an autoregulatory feedback loop that establishes expression of ELF3 and HLA-C in trophoblasts. Wrenchnolol blocked binding of MED23 to ELF3, thus disrupting the positive feedback loop that drives ELF3 expression, with down regulation of HLA-C expression as a consequence.

2021-01-27 | GSE165511 | GEO

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