GEO series

KLF13 promotes SLE Pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes [ATAC-seq]

GSE278048 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 28 samples Submitted 2024/10/15 Platform GPL21626

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 28 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: Mus musculus (mouse)
Samples: 28 samples: 28 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: KLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genesCommunications biology · 2024

Summary (written by the submitters)

Although significant progress has been achieved in elucidating the genetic architecture of systemic lupus erythematosus (SLE), identifying genes underlying the pathogenesis has been challenging. The NZM2410-derived lupus susceptibility Sle3 locus is associated with T cell hyperactivity and activated myeloid cells. However, candidate genes associated with these phenotypes have not been identified.

Read the full summary ↓

Here, we narrow the Sle3 locus to a smaller genomic segment (Sle3k) and show that mice carrying Sle3k and Sle1 loci developed lupus nephritis. We identify Klf13 as the primary candidate gene upregulated in Sle3k mice and demonstrate that Klf13 upregulation is associated with genome-wide transcription changes resulting in higher levels of proinflammatory cytokines, enhanced T cell activation, and hyperresponsiveness of myeloid cells. Correspondingly, Klf13 –/– mice display striking repression of genes involved in mediating immune activation, including key proinflammatory cytokines/chemokines. Furthermore, Klf13 –/– mice show profound dysregulation in cytokine signaling pathways in myeloid cells in response to toll receptor ligands, thus revealing a key role of KLF13 in modulating myeloid cell function. Klf13 upregulation is associated with increased production of RANTES, a key chemokine in lupus nephritis, in activated T cells and the kidneys of lupus-prone mice. In sum, our findings reveal Klf13 as a key gene in the Sle3 interval in mediating lupus pathogenesis that may have implications in the rational design of new therapies for SLE and other autoimmune/inflammatory diseases.

Published in

KLF13 promotes SLE pathogenesis by modifying chromatin accessibility of key proinflammatory cytokine genes

Wang A, Fairhurst AM, Liu K et al. · Communications biology 2024 · PMID 39506084 · doi:10.1038/s42003-024-07099-0

This dataset

Open GSE278048 in finder → Find more mouse 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 GSE278048_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 PRJNA1165276 and SRA study SRP534791. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39506084) ↗

Study design

28 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 28 sample titles: 28 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

GSM8538732 B6_T, replicate 1, ATAC-seq
GSM8538733 B6_T, replicate 2, ATAC-seq
GSM8538734 Sle3k_T, replicate 1 ATAC-seq
GSM8538735 Sle3k_T, replicate 2 ATAC-seq
GSM8538736 B6_M, replicate 1, ATAC-seq
GSM8538737 B6_M, replicate 2, ATAC-seq
GSM8538738 Sle3k_M, replicate 1, ATAC-seq
GSM8538739 Sle3k_M, replicate 2, ATAC-seq
GSM8538740 WT_T, replicate 1, ATAC-seq
GSM8538741 WT_T, replicate 2, ATAC-seq
GSM8538742 KLF13-/-_T, replicate 1, ATAC-seq
GSM8538743 KLF13-/-_T, replicate 2, ATAC-seq
GSM8538744 WT_T1, replicate 1, ATAC-seq
GSM8538745 WT_T1, replicate 2, ATAC-seq
GSM8538746 KLF13-/-_T1, replicate 1, ATAC-seq
GSM8538747 KLF13-/-_T1, replicate 2, ATAC-seq
GSM8538748 WT_M, replicate 1, ATAC-seq
GSM8538749 WT_M, replicate 2, ATAC-seq
GSM8538750 KLF13-/-_M, replicate 1, ATAC-seq
GSM8538751 KLF13-/-_M, replicate 2, ATAC-seq
GSM8538752 WT_D1, replicate 1, ATAC-seq
GSM8538753 WT_D1, replicate 2, ATAC-seq
GSM8538754 KLF13-/-_D1, replicate 1, ATAC-seq
GSM8538755 KLF13-/-_D1, replicate 2, ATAC-seq
GSM8538756 WT_D2, replicate 1, ATAC-seq
GSM8538757 WT_D2, replicate 2, ATAC-seq
GSM8538758 KLF13-/-_D3, replicate 1, ATAC-seq
GSM8538759 KLF13-/-_D3, replicate 2, ATAC-seq

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GSE246700 Regulatory T cells in the Tumor Microenvironment Display a Unique Chromatin Accessibility Profile (ATAC-Seq) 140 samples shares accessibility, chromatin
GSE296014 Post-replicative chromatin accessibility predicts cell fate change. 81 samples shares accessibility, chromatin
GSE216371 A single-cell atlas of chromatin accessibility in mouse organogenesis 68 samples shares accessibility, chromatin
GSE242799 Effect of SWI/SNF pertubations on chromatin accessibility during macrophage inflammatory activation [ATAC-seq] 40 samples shares accessibility, chromatin

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