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The Integrator complex is required for optimal lytic lifecycle of Kaposi’s Sarcoma-Associated Herpesvirus [ChIP-seq]

GSE300544 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2025/06/25 Platform GPL34281
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 16 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
16 samples: 2 × INTS11 ChIP-seq, 0h, vs 2 × INTS11 ChIP-seq, 24h, vs 2 × INTS11 ChIP-seq, 48h, vs 2 × INTS11 ChIP-seq, 72h,Groups 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.
Summary (written by the submitters)
The Integrator complex (INT) is an essential regulator of RNA biogenesis across evolution. Most current findings describe INT’s function in states of equilibrium, presenting a research gap in INT’s role in dynamic states, such as in infections and cancers. Viruses hijack cellular RNA machinery to transcribe their genes and produce viral progeny, presenting a unique condition to investigate INT-dependent RNA regulation under perturbation.
Read the full summary ↓
Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic DNA virus that causes two deadly cancers, Kaposi’s sarcoma and primary effusion lymphoma. KSHV undergoes a highly regulated and robust transcription of viral genes upon lytic reactivation, providing a complex and dynamic system to investigate Integrator-mediated viral/host RNA metabolism. We find that Integrator subunit 11 (INTS11), the enzymatic core of INT, is required for an optimal KSHV lytic lifecycle following reactivation from latency or after primary infection. While INTS11 knockdown’s impact on the human transcriptome remains bi-directional, it almost exclusively represses the KSHV transcriptome throughout the lytic stages. This inhibits viral protein expression, viral genome replication, and virion production. Integrator subunits 9 and 6 are also important for the KSHV lytic lifecycle. RNA-seq analyses revealed dynamic and unique signatures of human transcriptomes during each latent or lytic stage. Mechanistically, ChIP-seq analysis showed that INTS11 is broadly and increasingly recruited to the KSHV genome with unique binding site specificities as the lytic cycle progresses, suggesting that KSHV hijacks INTS11 to facilitate its lytic lifecycle. These findings reveal unexpected and critical roles of the Integrator complex in the lytic phase of KSHV infection.
This dataset
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.

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 GSE300544_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1281158 and SRA study SRP594024. Searching any of these in the dataset finder brings you back here.

Study design
2 × INTS11 ChIP-seq, 0h, vs 2 × INTS11 ChIP-seq, 24h, vs 2 × INTS11 ChIP-seq, 48h, vs 2 × INTS11 ChIP-seq, 72h,

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 8 of them. 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
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