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The divergent role of two PRDM1 isoforms during human naïve pluripotency reprogramming [ATAC-seq]

GSE255859 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 31 samples Submitted 2024/11/29 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 31 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
31 samples: 15 conditions, mostly in duplicateGroups 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)
Induced pluripotent stem cells (iPSCs) technology offers great promise for scientific research and clinical applications. iPSCs can be generated from various cell types through different strategies. Two different pluripotent states, naive and primed, can be captured in vitro, corresponding to the pre- and post-implantation stages of in vivo development, respectively, with naive pluripotency being considered to possess better developmental potential.
Read the full summary ↓
We can obtain naïve iPSCs and primed iPSCs through somatic cell reprogramming. Despite well-characterized transcriptional and epigenetic changes, the dynamic of the chromatin landscape during naïve and primed iPSC reprogramming is poorly understood, especially in humans. In this study, we applied ATAC-seq and RNA-seq to delineate the chromatin landscape in the human secondary reprogramming system towards naive and primed pluripotency. We identified several transcription factors and epigenetic factors which were crucial to reprogramming chromatin remodeling. We found that two isoforms of the same gene PRDM1, PRDM1α and PRDM1β, targeted different genomic loci to function in divergent roles during naive reprogramming. We proposed a cross-regulation model of PRDM1α and PRDM1β function. Together, this research highlights the diversity of the transcription factors in determining the chromatin landscape dynamics and regulating pluripotent cell fates.
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 GSE255859_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 PRJNA1077081 and SRA study SRP490038. Searching any of these in the dataset finder brings you back here.

Study design
15 conditions, mostly in duplicate
ATAC-seq_2d ×3 ATAC-seq_hiF-T ×2 ATAC-seq_6d ×2 ATAC-seq_n8d ×2 ATAC-seq_n14d ×2 ATAC-seq_n20d ×2 ATAC-seq_n24d ×2 ATAC-seq_n24d+dox ×2 +7 more

Supports a between-group comparison across 31 samples.

How we read this: 15 replicated groups read from 31 sample titles; they account for 31 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
Datasets on a similar topic

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