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

ABSTRACT: Temporal-spatial Establishment of Initial Niche for the Primary Spermatogonial Stem Cell formation is Determined by an ARID4B Regulatory Network

PROVIDER: PRJNA331161 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3950704_1.fastq.gz	Fastqsanger.gz
	SRR3950704_2.fastq.gz	Fastqsanger.gz
	SRR3950695.fastq.gz	Fastqsanger.gz
	SRR3950705_1.fastq.gz	Fastqsanger.gz
	SRR3950705_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

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.

2017-03-27 | GSE84802 | GEO

Temporal-spatial Establishment of Initial Niche for the Primary Spermatogonial Stem Cell formation is Determined by an ARID4B Regulatory Network (RNA-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 RNA-Seq analysis to examine the gene expression profile of the Arid4bSCKO testes in comparison with that of control testes.

2017-03-27 | GSE84804 | GEO

Temporal-Spatial Establishment of Initial Niche for the Primary Spermatogonial Stem Cell Formation Is Determined by an ARID4B Regulatory Network.

Project description:During neonatal testis development, centrally located gonocytes migrate to basement membrane of the seminiferous cords, where physical contact with a niche established by Sertoli cells is essential for transition of gonocytes into spermatogonial stem cells (SSCs). To provide structural support and signaling stimuli for the gonocyte-to-SSC transition that occurs at a specific location during a finite phase, temporal-spatial establishment of the niche is critical. To date, the factors that guide Sertoli cells to establish the initial stem cell niche remain largely unknown. Using the Sertoli cell-specific Arid4b knockout (Arid4bSCKO) mice, we demonstrated that ablation of AT-rich interaction domain 4B (ARID4B) resulted in abnormal detachment of Sertoli cells from the basement membrane of seminiferous cords during the gonocyte-to-SSC transition phase, suggesting failure to establish a niche for the SSC formation. Without support by a niche environment, gonocytes showed disarranged cell distribution in the Arid4bSCKO testes and underwent apoptosis. The commitment of gonocytes to differentiate into the spermatogonial lineage was broken and the capability of SSCs to self-renew and differentiate was also impaired. Gene expression profiling revealed the molecular mechanisms responsible for the phenotypic changes in the Arid4bSCKO testes, by identifying genes important for stem cell niche function as downstream effectors of ARID4B, including genes that encode gap junction protein alpha-1, KIT ligand, anti-Müllerian hormone, Glial cell-line derived neurotrophic factor, inhibin alpha, inhibin beta, and cytochrome P450 family 26 subfamily b polypeptide 1. Our results identified ARID4B as a master regulator of a signaling network that governs the establishment of a niche during the critical gonocyte-to-SSC transition phase to control the fate of gonocytes and SSCs. Stem Cells 2017;35:1554-1565.

| S-EPMC5743547 | biostudies-literature

Identification of a Transcription Factor that Promotes Spermatogonial Stem Cell Establishment

Project description:Spermatogonial stem cells (SSCs) are critical for maintaining spermatogenesis throughout adult life. Little is known about how SSCs are first generated. Here, we report the identification of a transcription factor—RHOX10—that promotes the initial establishment of SSCs. We were led to this discovery because we found that conditional loss of a large X-linked gene cluster comprised of 33 related homeobox genes, including Rhox10, causes defects predicted if SSCs fail to be generated or maintained. Remarkably, KO of only Rhox10 elicits SSC-related defects indistinguishable from KO of the entire gene cluster. Using a battery of approaches, including single cell-RNAseq analysis, we determined that loss of Rhox10 causes accumulation of undifferentiated germ cells—Pro-spermatogonia (ProSG)—at a time when they normally would form SSCs. The identification of a transcription factor that drives the initial generation of SSCs has potential therapeutic applications for infertility.

2016-09-27 | GSE82174 | GEO

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

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

2017-03-27 | GSE84808 | GEO

Expression data from Arid4b knockdown cell lines

2012-04-24 | GSE35731 | GEO

Mus musculus

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

| PRJNA331163 | ENA

Mus musculus

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

| PRJNA331159 | ENA

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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