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Requisite chromatin remodeling for myeloid and erythroid lineage differentiation from erythromyeloid progenitors

ABSTRACT: The mammalian SWI/SNF chromatin-remodeling BAF (BRG1/BRM-associated factor) complex has an essential role in developmental and pathological processes. We show that deletion of Baf155 encoding a subunit of the BAF complex in the Tie2(+) lineage (Baf155 CKO) leads to defects in yolk sac myeloid and definitive erythroid (EryD) lineage differentiation from erythromyeloid progenitors (EMPs). The chromatin of myeloid gene loci in Baf155 CKO EMPs is mostly inaccessible and enriched mainly by the ETS binding motif. BAF155 interacts with PU.1 and is recruited to PU.1 target gene loci together with p300 and KDM6a. Treatment of Baf155 CKO embryos with GSK126, an H3K27me2/3 methyltransferase EZH2 inhibitor, rescues myeloid lineage gene expression. This study uncovers indispensable BAF-mediated chromatin remodeling of myeloid gene loci at the EMP stage. Future studies exploiting epigenetics in generation and application of EMP derivatives for tissue repair, regeneration, and disease are warranted.

ORGANISM(S): Mus musculus

PROVIDER: GSE144243 | GEO | 2020/11/17

REPOSITORIES: GEO

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Requisite chromatin remodeling for myeloid and erythroid lineage differentiation from erythromyeloid progenitors

Project description:The mammalian SWI/SNF chromatin-remodeling BAF (BRG1/BRM associated factor) complex plays an essential role in developmental and pathological processes. We show that the deletion of Baf155 encoding a subunit of BAF complex in the Tie2(+) lineage (Baf155 CKO) leads to defects in the yolk sac myeloid and definitive erythroid (EryD) lineage differentiation from erythromyeloid progenitors (EMPs) and embryonic lethality. Baf155 knock-down in EMP was sufficient to block myeloid and EryD differentiation. Chromatin of the myeloid gene loci in Baf155 CKO EMPs was largely inaccessible and was enriched mostly by the ETS binding motif. BAF155 interacted with PU.1 and was recruited to the PU.1 in target gene loci together with p300 and KDM6a. Treatment of Baf155 CKO embryos with GSK126, an inhibitor of the H3K27me2/3 methyltransferase EZH2, rescued myeloid lineage gene expression. These studies uncover the indispensable BAF mediated chromatin remodeling of the myeloid gene loci at the EMP stage.

2021-03-08 | GSE159381 | GEO

A human iPSC-derived multilineage liver organoid model containing Kupffer cells to study human sepsis-associated liver dysfunction [hiPSC-EMP-KC-pKC]

Project description:To incorporate Kupffer cells into hiPSC-LOs, we differentiated erythro-myeloid progenitors (EMPs) from hiPSCs. We compares the gene expression profiles of hiPSC-EMPs with cord-blood hematopoietic stem and progenitor cells (CB-HSPCs); and EMP-generated Kupffer cells (EMP-KC) with human primary Kupffer cells.

2024-03-01 | GSE233538 | GEO

Ezh2 is essential for the generation of functional yolk sac derived erythro-myeloid progenitor [CUT&RUN]

Project description:Yolk sac (YS) hematopoiesis is critical for the survival of the embryo and a major source of tissue-resident macrophages that persist into adulthood. Here we report that the epigenetic regulator Ezh2 is essential for YS hematopoiesis but dispensable for subsequent aorta–gonad–mesonephros (AGM) blood development. Loss of Ezh2 activity in hemogenic endothelium (HE) leads to the generation of phenotypically intact but functionally deficient erythro-myeloid progenitors (EMP). Ezh2 activity is critical at the onset of the endothelial-to-hematopoietic transition generating EMPs but rapidly dispensable after that. We identified a lack of downregulation of Wnt signaling as the primary reason in the generation of non-functional EMPs. Together, our findings demonstrate a critical and specific role of Ezh2 in modulating Wnt signaling during the generation of EMPs from YS HE.

2021-08-16 | GSE181869 | GEO

Ezh2 is essential for the generation of functional yolk sac derived erythro-myeloid progenitors [ATAC-seq]

2021-06-01 | GSE150292 | GEO

Ezh2 is essential for the generation of functional yolk sac derived erythro-myeloid progenitors [RNA-seq]

2021-08-16 | GSE150032 | GEO

Single cell transcriptome analysis of primary murine EMP reveals complex erythroid, myeloid, and innate lymphoid lineage heterogeneity

Project description:Single cell transcriptome analysis of primary murine EMP reveals complex erythroid, myeloid, and innate lymphoid lineage heterogeneity

2021-07-05 | GSE143871 | GEO

Chromatin remodeling BAF155 subunit regulates the genesis of basal progenitors in developing cortex

Project description:We have analyzed gene expression differences between control, BAF155 conditional knockout (cKO) and Pax6 cKO embryonic cortices at E15.5.

2018-05-11 | GSE114351 | GEO

BAF Complex Enhances Reprogramming of Adult Human Fibroblasts

Project description:Chromatin remodeling molecules of the BAF complex, Brg1 and Baf155, as well as other chromatin remodeling modeling molecules have been described to enhance Oct4, Sox2, Klf4 and c-Myc mediated reprogramming of mouse somatic cells into induced pluripotent stem cells (iPSCs). Brg1 maintains pluripotency of mouse embryonic stem cells (mESCs) by modulating the expression of pluripotency genes including Oct4 in synergism with LIF/STAT signaling. Interestingly, unlike mESCs, BAF complex in human embryonic stem cells (hESCs) is composed of both BAF155 and BAF170, where BAF170 plays a role in maintaining hESCs pluripotency. In this study, we describe that BRG1 and BAF155 enhance reprogramming of adult human fibroblasts. Overexpression of BAF155 does not affect pluripotency of hiPSCs as tested by global gene expression profiling as well as in vivo and in vitro assays. Additionally, these findings show that BRG1 and BAF155 expression can enhance reprogramming even in the absence of LIF/STAT signaling.

2018-11-29 | GSE75568 | GEO

The BAF chromatin remodeling complex regulates gene expression programs essential for mammalian neural crest development

Project description:Neural crest cells (NCCs) are a multipotent cell population that contributes to the development of many tissues including craniofacial, pharyngeal arch arteries, and cardiac outflow tract (OFT). The BAF complex plays an important role in the development of a wide range of tissues by modulating gene expression programs at the chromatin level. However, its role in neural crest development has remained unclear. To determine the role BAF complex, we deleted BAF155 and BAF170, the core subunits required for the assembly, stability, and functions of the BAF complex in NCCs. Mouse embryos lacking BAF155/170 in NCCs displayed early lethality due to a wide range of developmental defects including craniofacial defects, pharyngeal arch artery defects, and OFT defects. We observed reduced proliferation, increased cell death, and impaired migration of cardiac NCCs to the OFT in BAF155/170 mutants. RNAseq analysis on sorted NCCs revealed that the BAF complex regulates the expression of numerous genes essential for neural crest development. We observed downregulation of Hippo and Notch signaling pathways, both essential for the migration, proliferation, and differentiation of the NCCs. The BAF complex interacts with transcription factors to modulate the transcriptional program. Therefore, we performed transcription factor enrichment analysis on the RNAseq data set and identified several transcription factors including Hey1, Hey2, and Hes5 that may directly or indirectly interact with the BAF complex in NCCs. We also found that Brg1 interact with Tead transcription factors and the interaction was impaired in BAF155/170 knockdown cells. Together, our results demonstrate an important role of the BAF complex in modulating the gene regulatory network essential for neural crest development.

2021-03-05 | GSE153121 | GEO

Single-cell RNA sequencing of Cd45+ adventitial cells from mice at steady state or treated with AngiotensinII

Project description:Here we show, that arterial macrophages derive predominantly from YS EMPs, which give rise to a transcriptionally distinct cluster of macrophages with mainly homeostatic and anti-inflammatory properties in steady state as well as in response to AngII inflammation. In adult mice, these EMP-derived macrophages persist for long periods of time, but decreas in absolute numbers in senescence without compensation by BM-derived progenitors. EMP-derived macrophages expressed high levels of homeostatic genes such as Lyve-1, which links them to physiological functions in arteries.

2020-08-04 | GSE155569 | GEO

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