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The role of DPF2 in mouse radiation-induced intestinal injury [scRNA-seq]

ABSTRACT: We have employed a single-cell sequencing approach using 10x Genomics ScRNA-seq to study the role of DPF2 in immune cells of Radiation-induced intestinal injury (RIII). The intestinal immune system has been increasingly recognized for their roles in regulating intestinal inflammation. This study represents the SWI/SNF chromatin-remodeling subunit DPF2 mediates the inflammatory network in intestinal injury and provides new insights in RIII.

ORGANISM(S): Mus musculus

PROVIDER: GSE289938 | GEO | 2025/10/07

REPOSITORIES: GEO

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The role of DPF2 in mouse radiation-induced intestinal injury by spatial transcriptome

Project description:We have employed spatial transcriptomes to study the role of DPF2 in macrophages of Radiation-induced intestinal injury (RIII). The intestinal macrophage has been increasingly recognized for their roles in regulating intestinal inflammation. This study represents the SWI/SNF chromatin-remodeling subunit DPF2 mediates the inflammatory network in intestinal injury and provides new insights in RIII.

2025-10-07 | GSE290563 | GEO

The role of DPF2 in mouse radiation-induced intestinal injury by ATAC-seq

Project description:We have employed ATAC-seq to study the role of DPF2 in intestinal immune cells. The intestinal immune cells have been increasingly recognized for their roles in regulating intestinal inflammation. This study represents the SWI/SNF chromatin-remodeling subunit DPF2 mediates the inflammatory network in intestine.

2025-10-07 | GSE290650 | GEO

The study of dpf2 in mouse ES cells

Project description:Brg-or Brm-associated factor (BAF) complexes, is a 12 subunit complex which contains an ATPase subunit, Brg or Brm, that uses energy derived from ATP hydrolysis to disrupt histone:DNA contacts to catalyze transcriptional events such as promoting gene expression or repression. Genetic studies in mice demonstrated that BAF complexes are essential for early embryonic development and pluripotency. ES cells express distinctive compleses, termed esBAF complexes by the presence of BAF155, Brg, BAF60a. Purification of Brg and Brm-associated proteins reveals a new family of four stoichiometric subunits of mSWI/SNF or BAF complexes which was termed BAF45a, b, c, and d. The progenitors to both neurons and glia are maintained in a proliferative state by a specified SWI/SNF-like npBAF complex that contains both BAF45a and BAF53a. The transition from proliferative to neurogenic divisions requires the exchange of these subunites for the homologous BAF45b or BAF45c and BAF53b proteins. The function of BAF45d remwains unclear so far.At present, we found that the knockout of dpf2 in ES cells impared the differention of ES cells. We will identify the target genes of dpf2 by Chip-seq so that we could study how dpf2 affect the differentiation of ES cells into germ layers.Protocol: DNA was prepared from ES cells by standard ChIP method. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2013-09-30 | E-ERAD-24 | biostudies-arrayexpress

The role of DPF2 in mouse radiation-induced intestinal injury [scRNA-seq]

Project description:The role of DPF2 in mouse radiation-induced intestinal injury [scRNA-seq]

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Single-Cell Map of Dynamic Multicellular Ecosystem of Radiation-Induced Intestinal Injury

Project description:Using single-cell RNA sequencing, we pictured a dynamic landscape of the intestinal microenvironment during RIII and regeneration. We generated transcriptomes of 22,680 single cells in the intestinal microenvironment, trying to profile the dynamics of ISCs and immune cells located in the mucous layer. This large-scale single-cell transcriptome data can be used as a valuable resource for further studying the cellular mechanism of RIII and development of potential therapy strategies.

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The role of DPF2 in mouse radiation-induced intestinal injury by ATAC-seq

Project description:The role of DPF2 in mouse radiation-induced intestinal injury by ATAC-seq

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The role of DPF2 in mouse radiation-induced intestinal injury by spatial transcriptome

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The SWI/SNF subunit Dpf2 licenses Nrf2-dependent gene expression to enforce multilineage control of inflammation [ChIP-seq]

Project description:Purpose: Multi-omics characterization of the consequences of deleting the SWI/SNF subunit Dpf2 in the transcriptome (RNAseq), accessibility of the genome (ATACseq) and binding of SWI/SNF subunits (CUT&RUN) in hematopoietic stem/progenitor cells, resting and polarized bone-marrow derived macrophages and resting and activated CD4+ T cells obtained from Dpf2f/f and Dpf2D/D mice. Methods: Lin- cKit+ cells were sorted from bone marrow of 28-days old Dpf2f/f and Dpf2D/D mice. Bone-marrow derived macrophages were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and polarized with IFNg and LPS, or IL-4 for 24hours. CD4+ splenic T helper cells were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and activated by treatment with PMA and Ionomycin. Methods: For ChIPseq in SKNO1 cell lines (AML), 10 million SKNO1 cells carrying shLuciferase or shDpf2#2487 were grown in the presence of doxycycline for 7 days to induce Dpf2 depletion. At day 7 of culture, cells were crosslinked with 1% formaldehyde for 15 minutes, quenched with 125mM Glycine for 5 minutes, washed in PBS and flash frozen at -80C. Crosslinked cell pellets were processed for ChIPseq following a previously described protocol (Boulay G et al., Cell 2017). Results: For ChIPseq, reads were trimmed using Cutadapt (v1.15--nextseq-trim=20 -m 18), aligned to the Human h38 genome using BWA (v0.7.13) with parameters aln -q 5 -l 32 -k 2, and deduplicated using Picard Mark Duplicates (v2.10.6). Peaks were called using narrow peaks by macs2 (v2.1.1.20160309) with IgG used as background. Conclusions: The absence of Dpf2 in LK cells results in downregulation of anti-oxidative and anti-inflammatory gene expression programs in bone marrow LK cells, bone-marrow derived macrophages and CD4+ T cells.

2023-06-06 | GSE192778 | GEO

The SWI/SNF subunit Dpf2 licenses Nrf2-dependent gene expression to enforce multilineage control of inflammation [ATAC-seq]

Project description:Purpose: Multi-omics characterization of the consequences of deleting the SWI/SNF subunit Dpf2 in the transcriptome (RNAseq), accessibility of the genome (ATACseq) and binding of SWI/SNF subunits (CUT&RUN) in hematopoietic stem/progenitor cells, resting and polarized bone-marrow derived macrophages and resting and activated CD4+ T cells obtained from Dpf2f/f and Dpf2D/D mice. Methods: Lin- cKit+ cells were sorted from bone marrow of 28-days old Dpf2f/f and Dpf2D/D mice. Bone-marrow derived macrophages were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and polarized with IFNg and LPS, or IL-4 for 24hours. CD4+ splenic T helper cells were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and activated by treatment with PMA and Ionomycin. Methods: For ATACseq, Lin- cKit+ cells were processed following the OMIM-ATAC-seq protocol (Corces MR et al., Nature Methods 2017). Libraries were sequenced on a NextSeq (75bp, paired end reads) to obtain more than 40 million reads/sample. Results: For ATACseq, we obtained more than 40 million reads per sample. ATAC-Seq chromatin accessible regions were determined using ENCODE pipeline standards (https://github.com/ENCODE-DCC/atac-seq-pipeline; git commit 2b693ab). Conclusions: The absence of Dpf2 in LK cells results in downregulation of anti-oxidative and anti-inflammatory gene expression programs in bone marrow LK cells, bone-marrow derived macrophages and CD4+ T cells.

2023-06-06 | GSE192776 | GEO

The SWI/SNF subunit Dpf2 licenses Nrf2-dependent gene expression to enforce multilineage control of inflammation [RNA-seq]

Project description:Purpose: Multi-omics characterization of the consequences of deleting the SWI/SNF subunit Dpf2 in the transcriptome (RNAseq), accessibility of the genome (ATACseq) and binding of SWI/SNF subunits (CUT&RUN) in hematopoietic stem/progenitor cells, resting and polarized bone-marrow derived macrophages and resting and activated CD4+ T cells obtained from Dpf2f/f and Dpf2D/D mice. Methods: Lin- cKit+ cells were sorted from bone marrow of 28-days old Dpf2f/f and Dpf2D/D mice. Bone-marrow derived macrophages were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and polarized with IFNg and LPS, or IL-4 for 24hours. CD4+ splenic T helper cells were obtained from 28-days old Dpf2f/f and Dpf2D/D mice and activated by treatment with PMA and Ionomycin. Methods: For RNAseq, total RNA was extracted using RNEasy Plus micro kit (Qiagen). Ribosomal RNA was removed using NEBNext rRNA Depletion kit and RNAseq libraries were prepared using Illumina's TruSeq total stranded RNAseq prep kit (NuGEN Technologies). RNAseq libraries were sequenced on an Illumina NextSeq500 prep kit (Paired-end, 75bp) or NovaSeq 6000. Results: For RNAseq samples, we obtained more than 40 million paired-end reads per sample. Reads were aligned to the mm10 transcriptome and ERCC spike-in indexes using RSEM (v1.3.0) and STAR (v2.6.0c) with Gencode annotations. Differentially expressed genes were determined by DESeq2 (v1.18.1, Wald Test, p-adj<0.05) after gene counts were corrected based on ERCC variances using RUVseq (v1.12.0). Conclusions: The absence of Dpf2 in LK cells results in downregulation of anti-oxidative and anti-inflammatory gene expression programs in bone marrow LK cells, bone-marrow derived macrophages and CD4+ T cells.

2023-06-06 | GSE192775 | GEO

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