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Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B [ChIP-seq]

ABSTRACT: Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B [ChIP-seq]

PROVIDER: PRJNA623629 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11506592.fastq.gz	Fastqsanger.gz
	SRR11506593.fastq.gz	Fastqsanger.gz

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Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B [ChIP-seq]

Project description:Hematopoiesis is maintained by a highly regulated and hierarchical system, whereas aberrant control of hematopoiesis is the underlying cause of severe hematological diseases. Here, we demonstrate the indispensable role of ARID4B in fetal hematopoiesis that recruits Ezh2 to transcriptionally downregulate the expression of KIT during erythroid cell differentiation. Functional analyses reveal that the aberration of Arid4b inhibits fetal hematopoiesis at the multipotent progenitors (MPPs) stage, which reactivates the KIT-Src-family kinase (Src) pathway and leads to pre-mature erythroblast proliferation. The differentiation defect caused by ARID4B aberration could be counteracted by the Src inhibitor PP2 or by KIT knockdown. In summary, we identify ARID4B as a master regulator in the KIT-Src pathway, thus providing a fundamental insight in hematopoiesis and stem cell regulation.

2021-11-09 | GSE148272 | GEO

Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B [RNA-seq]

2021-11-09 | GSE148269 | GEO

Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B

Project description:Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B

| PRJNA623628 | ENA

Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B [RNA-seq]

Project description:Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B [RNA-seq]

| PRJNA623630 | ENA

Inhibiting the KIT-Src pathway to ensure differentiation of hematopoietic progenitor requires ARID4B

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-11-06 | GSE148273 | GEO

Differentiation of fetal hematopoietic stem cells requires ARID4B to restrict autocrine KITLG/KIT-Src signaling.

Project description:Balance between the hematopoietic stem cell (HSC) duality to either possess self-renewal capacity or differentiate into multipotency progenitors (MPPs) is crucial for maintaining homeostasis of the hematopoietic stem/progenitor cell (HSPC) compartment. To retain the HSC self-renewal activity, KIT, a receptor tyrosine kinase, in HSCs is activated by its cognate ligand KITLG originating from niche cells. Here, we show that AT-rich interaction domain 4B (ARID4B) interferes with KITLG/KIT signaling, consequently allowing HSC differentiation. Conditional Arid4b knockout in mouse hematopoietic cells blocks fetal HSC differentiation, preventing hematopoiesis. Mechanistically, ARID4B-deficient HSCs self-express KITLG and overexpress KIT. As to downstream pathways of KITLG/KIT signaling, inhibition of Src family kinases rescues the HSC differentiation defect elicited by ARID4B loss. In summary, the intrinsic ARID4B-KITLG/KIT-Src axis is an HSPC regulatory program that enables the differentiation state, while KIT stimulation by KITLG from niche cells preserves the HSPC undifferentiated pool.

| S-EPMC8722094 | biostudies-literature

Expression data from Arid4b knockdown cell lines

Project description:High Arid4b promotes mammary tumor growth and metastasis in mouse model systems, and is associated with poor metastasis-free survival in human breast cancer patients. Through shRNA-mediated knockdown, we demonstrated that loss of Arid4b significantly inhibits the ability of mouse breast cancer cells to metastasize to the lungs. We performed microarray expression and subsequent network analysis to identify genes diferentially regulated as a consequence of Arid4b knockdown. The highly metastatic mouse breast cancer cell line 6DT1 was transduced with lentiviral shRNAs targeting Arid4b (RMM4534-NM_194262, Open Biosystems) or scrambled control in the same pLKO.1 vector backbone. Stably transduced cells were selected with puromycin, then total RNA was isolated from pooled clones.

2012-04-23 | E-GEOD-35731 | biostudies-arrayexpress

Temporal-spatial Establishment of Initial Niche for the Primary Spermatogonial Stem Cell formation is Determined by an ARID4B Regulatory Network (ChIP-Seq)

Project description:The primary spermatogonial stem cells (SSCs), which arise from gonocytes during neonatal development, serve as a foundational self-renewing reservoir to ensure continuous production of spermatozoa throughout adulthood. The transformation of gonocytes into SSCs takes place in a niche established by Sertoli cells. To date, the factors that guide Sertoli cells to establish the initial stem cell niche remain largely unknown. Using Sertoli cell-specific Arid4b knockout (Arid4bSCKO) mice, we demonstrated that ablation of ARID4B resulted in failure to establish a niche for the SSC formation. We performed ChIP-Seq analysis to identify target genes of ARID4B in testes.

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Expression data from Arid4b knockdown cell lines

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The role of Arid4b in mESC lineage commitment (ChIP-Seq)

Project description:Distinct cell types emerge from embryonic stem cells through a precise and coordinated execution of gene expression programs during lineage commitment. This is established by the action of lineage specific transcription factors along with chromatin complexes. Numerous studies focused on epigenetic factors that affect ESC self-renewal and pluripotency. However, the contribution of chromatin to lineage decisions at the exit from pluripotency has not been studied extensively. We have set out to identify chromatin related factors critical for differentiation towards mesodermal and endodermal lineages. Our results reveal a critical role for chromatin protein, Arid4b. Arid4b deficient mESCs are similar to wild-type mESCs in the expression of pluripotency factors and their self-renewal. However, we found that Arid4b loss results in defects in upregulation of meso/endodermal gene expression program. Arid4b is in the Sin3a complex along with Hdac1 and Hdac2. We identified a physical and functional interaction of Arid4b with Hdac1 rather than Hdac2. Arid4b deficiency leads to changes in the overall chromatin environment. Most notably, a subset of the genomic loci was found to gain H3K27Ac whereas several of the key developmental genes instead have increased H3K27me3 levels. Accordingly, the super-enhancers associated with meso/endoderm commitment were selectively reduced in arid4b∆ cells.

2020-10-20 | GSE153634 | GEO

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