GEO series
Tracing functional (epi)genomic imprints and their evolutionary origins in human defense antiviral cellular response (ChIP-seq III)
GSE288595
Homo sapiens; Mus musculus
Genome binding/occupancy profiling by high throughput sequencing
14 samples
Submitted 2025/02/24
Platform GPL24676Platform GPL24247
Summary
An integral part of human cellular homeostasis substantially relies on defense transcriptional responses tailored to fight microbial pathogens, including Viruses. However, a definitive anatomy of the “virus-responsive” fates of the non-coding genome was largely elusive. Here, we exhaustively assayed the human transcriptome and epigenome under naïve and antiviral cellular states and defined remarkable reprogramming to mark the exchange of cellular fates, involving previously unspecified, unsupervised, or overlooked non-coding entities endowed with thousands of novel virus-responsive enhancers, Super-enhancers (SEs), and Repetitive DNA enhancers. These functional determinants demonstrate superior chromatin architecture, stimulus-specificity, and transcriptional fitness, and neighbor, reside proximal, or entirely coincide with hundreds of the virus-stimulated genes, while a multitude of those is bound by the master antimicrobial TFs, IRF3 or/and NFκB, upon cell infection. A plethora of these DNA elements is traced within the repetitive fate of the human genome including Simple Tandem Repeats (STRs), Dispersed Repeats (DRs) such as retrotransposons and DNA transposons, and chimeras of those, enriched in HCTFBSs recognized by IRF3 or/and NFκB and exhibits pervasive imprints in the genomes of evolutionary recent, old and ancient species, including viruses. These findings emphasize the role of the architectural and functional compartmentalization of the human epigenome in naïve and infected cells on the perplexing natural conflicts and mechanistic dependencies that impose the frontage of defense gene expression in humans.
Published in
Koutsi MA, Pouliou M, Chatzopoulos D et al.
· Nucleic acids research 2025
· PMID 40131776
· doi:10.1093/nar/gkaf207
This dataset
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Direct links to NCBI, no account and no request form: the whole study as GSE288595_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 14 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1218652 and SRA study SRP561231. Searching any of these in the dataset finder brings you back here.
Study design
14 conditions, each sampled once — no replicated groups
Read from 14 sample titles: 14 distinct titles with little repetition. Check it against the sample list below before relying on it.
Samples in this study
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- GSM8770452 H3K27ac-ChIP-seq_A549_SVI_0h_2025
- GSM8770453 H3K27ac-ChIP-seq_A549_SVI_6h_2025
- GSM8770454 H3K27ac-ChIP-seq_NIH3T3_SVI_0h_2025
- GSM8770455 H3K27ac-ChIP-seq_NIH3T3_SVI_6h_2025
- GSM8770456 H3K27ac-ChIP-seq_THP-1_SVI_0h_2025
- GSM8770457 H3K27ac-ChIP-seq_THP-1_SVI_6h_2025
- GSM8770458 IRF3-ChIP-seq_A549_SVI_0h_2025
- GSM8770459 IRF3-ChIP-seq_A549_SVI_6h_2025
- GSM8770460 Input-ChIP-seq_A549_SVI_0h_2025
- GSM8770461 Input-ChIP-seq_A549_SVI_6h_2025
- GSM8770462 Input-ChIP-seq_NIH3T3_SVI_0h_2025
- GSM8770463 Input-ChIP-seq_NIH3T3_SVI_6h_2025
- GSM8770464 Input-ChIP-seq_THP-1_SVI_0h_2025
- GSM8770465 Input-ChIP-seq_THP-1_SVI_6h_2025
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