Project description: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.
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.
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.
Project description:Gene function in cancer is often cell type-specific. The epithelial cell-specific transcription factor ELF3 is a documented tumour suppressor in many epithelial tumours yet displays oncogenic properties in others. Here, we show that ELF3 is an oncogene in the adenocarcinoma subtype of lung cancer (LUAD), providing genetic, functional, and clinical evidence of subtype specificity. We discover a region of focal amplification at chromosome 1q32.1 encompassing the ELF3 locus in LUAD which is absent in the squamous subtype. Gene dosage and promoter hypomethylation affect the locus in up to 80% of LUAD analysed. ELF3 expression was required for tumour growth and a pan-cancer expression network analysis supports its subtype and tissue specificity. We further show that ELF3 displays strong prognostic value in LUAD but not LUSC. We conclude that, contrary to many other tumours of epithelial origin, ELF3 is an oncogene and putative therapeutic target in LUAD.
Project description:Temperature is a major environmental variable governing plant growth and development. ELF3 contains a polyglutamine (polyQ) repeat 8–10, embedded within a predicted prion domain (PrD). We find the length of the polyQ repeat correlates with thermal responsiveness. Plants from hotter climates appear to have lost the PrD domain, and these versions of ELF3 are stable at high temperature and lack thermal responsiveness. ELF3 temperature sensitivity is also modulated by the levels of ELF4, indicating that ELF4 can stabilise ELF3 function. This RNA-Seq dataset provides evidence for the hypothetical ELF3 function of temperature sensing .
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.
Project description:Our data showed that ELF3-AS1 was a nuclear lncRNA, and its biofunction in cancers is largely unknown to date. To explore the function of lncRNA ELF3-AS1 in gastric cancer, loss-of-function study was performed in SGC7901 and AGS cell lines. RNA sequencing studies showed that the expression of almost all the histone coding genes were significantly increased after knocking down of ELF3-AS1 in SGC7901 and AGS cell lines.
Project description:In Arabidopsis, ELF3, ELF4 and LUX proteins form the EC complex. The EC complex binds directly to the promoters of PIF4 and PIF5 in vivo, thereby inhibiting PIF4 and PIF5 expression at night. PIF4, as a key transcription factor for light and temperature, binds to thousands of target genes to regulate their expression. High temperature can activate PIF4 activity, making it regulate plant thermal morphogenesis by integrating light, circadian rhythm and hormone signals, EC complex is a protein complex that inhibits gene expression, and helps higher plants sense environmental temperature and thermal form. ELF3 is a thermal sensor that plays a role in controlling the circadian rhythm, photoperiodic flowering, hypocotyl length, and response to light in an EC-dependent and EC-independent manner. PIF4 plays a key positive role in heat response gene expression and hypocotyl growth in Arabidopsis thaliana, but ELF3 negatively regulates the protein activity of growth promoting factor PIF4. Interestingly, a 2020 paper published in Nature by Jung et al. found that ELF3, as a heat sensor, gradually forms multiple distinct spot-like structures in the nucleus as the temperature increases due to the presence of the characteristic PrD. Similarly, increasing the length of the polyQ will enlarge the spots. In addition, after returning to normal temperature from mild high temperature, the EC complex will quickly return to normal activity. This result is contrary to what Ronald et al. stated in a 2021 paper: Warm temperatures inhibit ELF3 blotching, and since ELF3 blotching is associated with increased transcriptional activity of ELF3, a decrease in blotching may lead to decreased EC function at warm temperatures. As a result, the question of how ELF3 is regulated in warmer temperatures remains an open question.