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The Nucleic Acid Binding Protein SFPQ Represses EBV Lytic Reactivation by Promoting Histone H1 Expression

GSE235265 Homo sapiens (human) RNA-seq (gene expression) 10 samples Submitted 2024/04/16 Platform GPL20301
At a glance

RNA-seq (gene expression) · human · 10 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Homo sapiens (human)
Samples
10 samples: 3 × sgControl vs 3 × SFPQKO_sg1 vs 2 × SFPQKO_sg2Groups 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
The nucleic acid binding protein SFPQ represses EBV lytic reactivation by promoting histone H1 expressionNature communications · 2024
Summary (written by the submitters)
Epstein-Barr virus (EBV) uses a biphasic lifecycle of latency and lytic reactivation to infect >95% of adults worldwide. Despite its central role in EBV persistence and oncogenesis, much remains unknown about how EBV latency is maintained. We used a human genome-wide CRISPR/Cas9 screen to identify that the nuclear protein SFPQ was critical for latency.
Read the full summary ↓
SFPQ supported expression of linker histone H1, which stabilizes nucleosomes and regulates nuclear architecture, but has not been previously implicated in EBV gene regulation. H1 occupied latent EBV genomes, including the immediate early gene BZLF1 promoter. Upon reactivation, SFPQ was sequestered into sub-nuclear puncta, and EBV genomic H1 occupancy diminished. Enforced H1 expression blocked EBV reactivation upon SFPQ knockout, confirming it as necessary downstream of SFPQ. SFPQ knockout triggered reactivation of EBV in B and epithelial cells as well as in Kaposi’s Sarcoma Associated Herpesvirus, suggesting a conserved gamma-herpesvirus role. These findings highlight SFPQ as a major regulator of H1 expression and EBV latency.
Published in
The nucleic acid binding protein SFPQ represses EBV lytic reactivation by promoting histone H1 expression
Murray-Nerger LA, Lozano C, Burton EM et al. · Nature communications 2024 · PMID 38755141 · doi:10.1038/s41467-024-48333-x
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 GSE235265_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA985633 and SRA study SRP445064. Searching any of these in the dataset finder brings you back here.

Study design
3 × sgControl vs 3 × SFPQKO_sg1 vs 2 × SFPQKO_sg2

Supports a between-group comparison across 8 samples.

How we read this: 3 replicated groups read from 10 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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