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DNA binding of ELF1 in A549 cells

ABSTRACT: DNA binding of ELF1 in A549 cells

PROVIDER: PRJNA503974 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10043569.fastq.gz	Fastqsanger.gz
	SRR10043570.fastq.gz	Fastqsanger.gz
	SRR10043571.fastq.gz	Fastqsanger.gz
	SRR10043572.fastq.gz	Fastqsanger.gz

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DNA binding of ELF1 in A549 cells

Project description:The goal of this study was to analyze the DNA binding landscape of ELF1 in A549 cells. We found that ELF1 mostly binds promoters of genes, close to transcription start sites. We used the promoter-bound genes from our ChIP-seq data and intersected it with differentially expressed genes upon ELF1 overexpression in A549 cells to identify a set of ELF1 regulated target genes.

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Elf1 promotes TC-NER in yeast by using its C-terminal domain to bind TFIIH

Project description:Transcription coupled-nucleotide excision repair (TC-NER) repairs DNA lesions that stall RNA polymerase II (Pol II) transcription. Here, we show that the C-terminal domain (CTD) of elongation factor-1 (Elf1) plays a critical role in TC-NER in yeast. Analysis of genome-wide repair of UV-induced cyclobutane pyrimidine dimers (CPDs) using CPD-seq indicates that the Elf1 CTD is required for efficient Rad26-dependent and Rad26-independent TC-NER across the yeast genome. The Elf1-CTD is also important for TC-NER in rad16∆ cells deficient in GG-NER. Finally, we show that a mutant in the Elf1-CTD (elf1-Y99A) that disrupts binding to a subunit of TFIIH affects Rad26-independent repair in a rad26∆ mutant background.

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A549 cells and MSR-A549 cells

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Project description:Purpose: Genome-wide DNA-binding analysis for Myocardin in human lung cancer cell line A549

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ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs [RNA-seq]

Project description:Aberrant overexpression of oncogenic ETS factors through chromosomal rearrangments is the most common genomic event in primary prostate tumor and these factors have been well studied. Loss of ELF1, another ETS transcription factor family member, is a common event in prostate cancer, but the function of ELF1 has not been described within the prostate. Studies of ELF1 in different tissue types has determined that it can be important for oncogeneis or tumor suppression. Here, we show that ELF1 is a novel prostate tumor suppressor by hindering oncogenic ETS function at cell migration related genes, but also that ELF1 has the ability to regulate senescence and chemotherapy resistance. Next generation sequencing was used to determine gene expression changes in RWPE-1 cells upon addition of an oncogenic ETS factor and then with the loss of ELF1 through an shRNA knockdown. Genomic binding locations were also determined for ELF1 and ERG, through ChIP-seq to identify any cobound or unique regions. The combination of this data indicates that ELF1 repressed migration related genes which ERG activates, but ELF1 also uniquely binds genes related to cell senescence and activates their transcription. There, these data indicate a novel tumor suppressive mechanism for ELF1 within the prostate and better characterizes its function within this cell type.

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ELF1 expression in prostate cells reduces oncogenic ETS functions and promotes senescence and sensitivity to chemotherapy through distinct gene expression programs [ChIP-seq]

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The ETS transcription factor ELF1 regulates a critical, broadly antiviral program distinct from the type I interferon response

Project description:Induction of vast transcriptional programs is a central event of innate host responses to viral infections. Here we report a unique transcriptional program with potent antiviral activity, driven by E74-like ETS transcription factor 1 (ELF1). Using high-content microscopy to quantify viral infection over time, we found that ELF1 inhibits eight diverse RNA and DNA viruses uniquely at multi-cycle replication. Elf1 deficiency results in enhanced susceptibility to influenza A virus infections in mice. ELF1 does not feed-forward to induce interferons, and ELF1’s antiviral effect is not abolished by the absence of STAT1 or by inhibition of JAK phosphorylation. Accordingly, comparative expression analyses by RNAseq revealed that the ELF1 transcriptional program is distinct from interferon signatures. Thus, ELF1 provides an additional layer of the innate host response, independent from the action of type I interferons.

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Project description:Two different groups of Ets transcription factors differentially act directly at the ZRS to define the spatial expression of Shh in the limb. Chromatin immunoprecipitation (ChIP) of Gabpa, Ets1, Etv4, Etv5 and Elf1 and by ChIP-on-chip analysis demonstrated that with the exception of Elf1 all bind directly to the Shh limb enhancer, the ZRS. Array design includes 2 biological replicates for Gabpa and Elf1, and two biological replicates and one dye swap replicate for Ets1, Etv4 and Etv5 samples.

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CPD-seq mapping of UV damage repair in elf1 mutant yeast

Project description:Elf1 is an important transcription elongation factor that has been implicated in transcription coupled-nucleotide excision repair (TC-NER). Here, we have used a high-throughput sequencing method known as CPD-seq to map the repair of UV-induced cyclobutane pyrimidine dimers (CPDs) at single nucleotide resolution across the yeast genome in elf1 mutant cells. Analysis of CPD repair indicates that Elf1 is important for CPD repair in the transcribed strand (TS) of yeast genes, indicating it plays an important role in TC-NER.

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