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Gene expression analyses in IRF8-induced monocyte differentiation

ABSTRACT: To understand the differentiation program in monocyte/macrophage differentiation, we performed ChIP-seq for IRF8 and H3K4me1 together with gene expression profiling during IRF8-induced monocyte differentiation. Both promoter-proximal and -distal binding of IRF8 associated with induction of the genes especially those related to monocytes/macrophages and immunity. DNA motif analysis for cis-regulatory elements of indirect IRF8 target genes predicted KLF4, essential for Ly6C+ monocyte development, to be a downstream transcription factor regulating the indirect target gene expression. Introduction of KLF4 into an Irf8-/- myeloid progenitor cell line induced a subset of IRF8 target genes and partially induced monocyte/macrophage differentiation. Together, this study revealed the genome-wide behavior of IRF8 and the IRF8-KLF4 axis during monocyte differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE38810 | GEO | 2013/01/24

SECONDARY ACCESSION(S): PRJNA168968

REPOSITORIES: GEO

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Gene expression analyses in IRF8-induced monocyte differentiation

Project description:To understand the differentiation program in monocyte/macrophage differentiation, we performed ChIP-seq for IRF8 and H3K4me1 together with gene expression profiling during IRF8-induced monocyte differentiation. Both promoter-proximal and -distal binding of IRF8 associated with induction of the genes especially those related to monocytes/macrophages and immunity. DNA motif analysis for cis-regulatory elements of indirect IRF8 target genes predicted KLF4, essential for Ly6C+ monocyte development, to be a downstream transcription factor regulating the indirect target gene expression. Introduction of KLF4 into an Irf8-/- myeloid progenitor cell line induced a subset of IRF8 target genes and partially induced monocyte/macrophage differentiation. Together, this study revealed the genome-wide behavior of IRF8 and the IRF8-KLF4 axis during monocyte differentiation. Gene expressions in monocyte-like cells differentiated by IRF8 or KLF4 were measured at day 4 after retroviral transductions to myeloid progenitor cell line, Tot2. Two independent experiments were performed.

2013-01-24 | E-GEOD-38810 | biostudies-arrayexpress

Monocyte Subsets with High Osteoclastogenic Potential and Their Epigenetic Regulation Orchestrated by IRF8 [RNA-Seq sorted cells]

Project description:Currently, it is unclear if all monocyte subsets exhibit osteoclastogenic potential. Furthermore, the role of lineage determining TFs in regulating OC differentiation on a genome-wide scale remains poorly understood. In this study, we utilized a novel Irf8 conditional knockout (Irf8 cKO) mouse model to characterize the importance of IRF8 in OC progenitor development and epigenetic regulation of OC differentiation. To identify global transcriptional program governing the osteoclastogenic potential of Ly6Chi, Ly6Cint, and Ly6C– monocytes, and how it may be further influenced by IRF8 deficiency, we performed RNA-seq on sorted Ly6Chi, Ly6Cint, and Ly6C– cells from WT and Irf8 cKO mice. Cells were analyzed prior to (BMMs) and 4 days after RANKL stimulation (OCs). Here we show that WT Ly6Chi and Ly6Cint monocytes developmentally contain OC-specific transcripts, which are augmented upon RANKL stimulation. Additionally, in the absence of IRF8, OC-specific transcripts in all three monocyte subsets are primed to robustly respond to RANKL stimulation.

2020-09-11 | GSE151480 | GEO

Genome wide profiling of active enhancers and IRF8-binding sites in murine mononuclear phagocyte lineage cells

Project description:To understand the mechanism underlying monocyte and dendritic cell development through the regulation of Irf8 expression by the 56 kb downstream (+56 kb) Irf8 enhancer, we performed epigenetic profiling of bone marrow cells and splenocytes from wild-type, the Irf8 +56 kb enhancer-deficient, and IRF8-deficient mice. Taken together with the transcriptome analysis of mononuclear phagocyte lineage cells in these mice, the Irf8 +56 kb enhancer-mediated high Irf8 expression in hematopoietic progenitor cells promote type 1 classical dendritic cell (cDC1) differentiation, while low Irf8 expression in progenitors led to Ly6C+ monocyte development. In addition, IRF8 ChIP-seq of mature cDC1s and monocytes suggested that IRF8 regulates enhancers in cooperation with different transcription factors in each lineage in its expression level.

2020-12-20 | GSE149757 | GEO

Project description:IRF8-induced monocyte differentiation

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Monocyte Subsets with High Osteoclastogenic Potential and Their Epigenetic Regulation Orchestrated by IRF8 [ChIP-Seq]

Project description:Currently, the epigenetic mechanisms governing the osteoclast differentiation process remains poorly understood. To investigate the combinatorial activity of TFs, cis-regulatory elements, and the enhancer landscape that establish and maintain osteoclast transcriptional identity, we profiled histone modifications (H3K4me1, H3K4me3, H3K27ac, H3K27me3) and PU.1 and IRF8 binding by ChIP-seq. RNA-seq data from sorted Ly6Chi, Ly6Cint, and Ly6C– cells were overlaid with ChIP-seq data to identify epigenetic changes specific to each subset and genotype. Our data suggest that the Ly6Chi inflammatory monocytes and Ly6Cint cells are transcriptionally and epigenetically programmed to differentiate in mature osteoclasts when compared to Ly6C– anti-inflammatory monocytes. A combinatorial activity of TFs and cis-regulatory elements in the vicinity of several osteoclast-specific genes are responsible for establishing and maintaining osteoclast identity in these subsets. In Irf8 cKO mice, several promoters and enhancers established during the progenitor stage may be critical for initiating early lineage commitment and priming monocyte subsets to differentiate into robust osteoclasts.

2020-09-19 | GSE151481 | GEO

Gene expression profiling in murine mononuclear phagocyte lineage cells

Project description:To understand the mechanism underlying monocyte and dendritic cell development through the regulation of Irf8 expression by the 56 kb downstream (+56 kb) Irf8 enhancer, we performed transcriptome analysis of bone marrow cells and splenocytes from wild-type, the Irf8 +56 kb enhancer-deficient, and IRF8-deficient mice. Taken together with the epigenetic profiling of mononuclear phagocyte lineage cells in these mice, the Irf8 +56 kb enhancer-mediated high Irf8 expression in hematopoietic progenitor cells promote type 1 classical dendritic cell (cDC1) differentiation, while low Irf8 expression in progenitors led to Ly6C+ monocyte development.

2020-12-20 | GSE149761 | GEO

Analysis of TF binding sites and histone modification in IRF8-induced monocyte differentiation

Project description:Chromatins were prepared from myeloid progenitor cell line Tot2 cells transduced with retrovirus for control MSCV or MSCV-IRF8. Chromatin immunoprecipitation (ChIP) was carried out by using anti-IRF8 antibody, anti-PU.1 antibody or anti-histone H3K4me1 antibody. ChIP-Seq peaks were identified using the FindPeaks tool in the HOMER package or SICER with input DNA tags as background distribution. Potential IRF8-direct target genes were identified based on ChIP-Seq and the alteration of expression by IRF8-induction. Examination of 2 transcription factor occupancy and 1 histone modifications in myeloid progenitor cells and monocyte-like cells differetiated by IRF8 expression

2013-01-24 | E-GEOD-38824 | biostudies-arrayexpress

Monocyte Subsets with High Osteoclastogenic Potential and Their Epigenetic Regulation Orchestrated by IRF8 [RNA-Seq]

Project description:Currently, it is unclear if all monocyte subsets exhibit osteoclastogenic potential. Furthermore, the role of lineage determining TFs in regulating OC differentiation on a genome-wide scale remains poorly understood. In this study, we utilized a novel Irf8 conditional knockout (Irf8 cKO) mouse model to characterize the importance of IRF8 in OC progenitor development and epigenetic regulation of OC differentiation. We performed RNA-seq on Irf8 gWT, gKO, cWT and cKO BMMs, preosteoclasts (PreOCs), and OCs. Cells were analyzed prior to (BMMs) and 3 days (PreOCs) and 6 days (OCs) after RANKL stimulation. Here we show that greater a number of genes are significantly upregulated in Irf8 cKO OCs when compared to WT and Irf8 gKO OCs. Altogether, our data shows that Irf8 cKO mice provide more precise/reliable OC-specific transcriptomic results when compared to Irf8 gKO mice.

2020-09-11 | GSE151388 | GEO

Mus musculus

Project description:Gene expression analyses in IRF8-induced monocyte differentiation

| PRJNA168968 | ENA

Fth1-mScarlet reports monocyte state during lipopolysaccharide-induced lung inflammation

Project description:Monocytes and macrophages are central to host defense but also contribute to inflammation-associated pathology. Efforts to manipulate monocyte and macrophage function are limited by our ability to effectively quantify the functional programs of these cells. We identified the gene Fth1, which encodes the Ferritin heavy chain, as highly predictive of alveolar macrophage transcriptomic states during LPS-induced lung inflammation and developed a novel Fth1-mScarlet reporter mouse. In the steady state lung, high Fth1-mScarlet expression is restricted to alveolar macrophages. In response to LPS-induced lung inflammation, Fth1 reporter activity is robustly increased in monocytes, with its expression reporting genes that are differentially expressed in monocytes versus macrophages. Consistent with this reporter associated gene profile, within the Lyz2-GFP+CD11b+Ly6C+ gate the highest Fth1 reporter expression was observed CD11c+ cells, indicative of monocyte-to-macrophage differentiation. While Fth1-mScarlet was induced in monocytes responding to either TLR4 ligation or M-CSF induced macrophage differentiation in vitro, TLR4-dependent expression occurred with greater speed and magnitude. Considering this, we suggest that Fth1-mScarlet expression reports monocyte-to-macrophage differentiation, with increased expression in pro-inflammatory states. Dissecting macrophage differentiation from inflammatory programs will be enhanced when combining Fth1-mScarlet with other reporter systems. Thus, the Fth1-mScarlet model addresses an important lack of tools to report the diverse spectrum of monocyte and macrophage states in vivo.

2024-09-25 | GSE278058 | GEO

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