GEO series

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [ChIP-Seq]

GSE208685 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2024/03/31 Platform GPL16791Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 12 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Homo sapiens (human)
Samples: 12 samples: 12 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1-bound enhancers through interactions with the EP400 chromatin remodelerNucleic acids research · 2024

Summary (written by the submitters)

Alu retrotransposons, forming the largest family of mobile DNA elements in the human genome, have recently come to attention as a potential source of regulatory novelties, most notably by participating in enhancer function. Even though Alu transcription by RNA polymerase III is subjected to tight epigenetic silencing, their bulk expression has long been known to increase in response to various types of stress, including viral infection.

Read the full summary ↓

Here we show that, in primary human fibroblasts, adenovirus small e1a triggered derepression of hundreds of individual Alus, by promoting TFIIIB recruitment by Alu-bound TFIIIC. Epigenome profiling revealed an e1a-induced decrease of H3K27 acetylation and increase of H3K4 monomethylation at derepressed Alus, making them resemble poised enhancers. The enhancer nature of e1a-targeted Alus was confirmed by the enrichment, in their upstream regions, of the EP300/CBP acetyltransferase and of the YAP1 and FOS transcription factors. The physical interaction of e1a with the chromatin remodeler EP400 turned out to be critical for Alu derepression, and upstream enrichment of EP400 was found to commonly demarcate expression-prone Alus. Our data suggest that e1a targets a subset of enhancer Alus whose transcriptional activation, mediated by e1a-EP400 interaction, may participate in the manipulation of enhancer activity by adenovirus.

Published in

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1-bound enhancers through interactions with the EP400 chromatin remodeler

Cantarella S, Vezzoli M, Carnevali D et al. · Nucleic acids research 2024 · PMID 39011896 · doi:10.1093/nar/gkae615

This dataset

Open GSE208685 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE208685_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA860610 and SRA study SRP387306. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39011896) ↗

Study design

12 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 12 sample titles: 12 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM6364235 IMR90, dl1500, BDP1, ChIP-seq
GSM6364236 IMR90, mock, BDP1, ChIP-seq
GSM6364237 IMR90, dl1500, RPC39, ChIP-seq
GSM6364238 IMR90, mock, RPC39, ChIP-seq
GSM6364239 IMR90, dl1500, TFIIIC, ChIP-seq
GSM6364240 IMR90, mock, TFIIIC, ChIP-seq
GSM8434430 input for dl312 infection of IMR90
GSM8434431 ChIP of BDP1 in dl312 infection of IMR90
GSM8434432 input for dl1500 infection of IMR90
GSM8434433 ChIP of BDP1 in dl1500 infection of IMR90
GSM8434434 input for p400b infection of IMR90
GSM8434435 ChIP of BDP1 in p400b infection of IMR90

Datasets on a similar topic

GSE208717 Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler 28 samples shares ep400, tead, ap-1, e1a, yap, transcription, interactions, adenovirus
GSE208716 Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [RNA-Seq] 16 samples shares ep400, tead, ap-1, e1a, yap, transcription, interactions, adenovirus
GSE66083 Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth 25 samples shares tead, ap-1, yap
GSE66082 Widespread association between YAP/TAZ/TEAD and AP-1 at enhancers drives oncogenic growth [gene expression] 12 samples shares tead, ap-1, yap
GSE295183 HIF2ɑ Requires Engagement with YAP/TAZ and AP-1 Transcription Factors to Maintain Oncogenic Transcription in Clear Cell Renal Cell Carcinoma [CUT&Tag] 60 samples shares ap-1, yap, transcription
GSE301506 YAP AND TEAD ARE TRANSCRIPTIONAL REGULATORS OF NEUROENDOCRINE DIFFERENTIATION AND GROWTH IN CARCINOID CELLS [ChIP-seq] 20 samples shares tead, yap, transcription
GSE306447 Aberrant Hippo-YAP/TEAD signaling drives malignant transcriptional reprogramming in external auditory canal squamous cell carcinoma 27 samples shares tead, yap, transcription
GSE269900 Identification of resistance mechanisms to small-molecule inhibition of YAP/TEAD-regulated transcription 18 samples shares tead, yap, transcription

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.