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Genome-wide map of SOX21 occupancy in human embryonic stem cell-derived neural progenitor cells [ChIP-seq]

ABSTRACT: To understand how SOX21 regulates neural fate specification, we differentiated wild type and SOX21 knockout hESC into neural epithelial cells (NECs) using dual SMAD inhibition protocol. We collected cells at neural differentiation day 5 and performed SOX21 ChIP-seq to investigate the genome-wide binding profiles. Meanwhile, we also carried out b-catenin ChIP-seq in wild type and SOX21 knockout NECs to dissect the role of SOX21 in Wnt signaling inhibition, thus providing important information for the mechanism underlying SOX21's functions in early neural fate specification.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110505 | GEO | 2019/10/28

REPOSITORIES: GEO

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SOX21 ensures rostral forebrain identity by suppression of WNT8B during neural regionalization of human embryonic stem cells

Project description:Generation of brain region-specific progenitors from human embryonic stem cells (hESCs) is critical for their application. However, transcriptional regulation of neural regionalization in human embryos is poorly understood. Here, we report that transcription factor SOX21 is required for telencephalic fate specification from hESCs. SOX21 knockout (KO) impairs telencephalic fate specification, concomitant with the activation of diencephalic genes and Wnt signaling. Inhibition of Wnt signaling restores telencephalic specification from SOX21 KO hESCs. Analysis of global SOX21 DNA binding profiles and SOX21-regulated genes identifies SOX21 targets. SOX21 interacts with b-catenin and interferes with TCF4/b-catenin binding to the enhancer of WNT8B. Double KO of SOX21 and WNT8B restores telencephalic specification, indicating that SOX21 specifies the telencephalic fate through repressing WNT8B expression. Moreover, the high and low levels of SOX21 in the telencephalon and diencephalon, respectively, in developing human brains support its role in telencephalic fate specification. Collectively, this study unveils previously unappreciated roles of SOX21 and sheds light on the transcriptional control of telencephalic patterning in humans.

2019-10-28 | GSE110504 | GEO

SOX21 ensures rostral forebrain identity by suppression of WNT8B during neural regionalization of human embryonic stem cells

2019-10-28 | GSE138094 | GEO

ChIP-seq on Olig2, Ascl1, Tcf3, Max, NFI, Sox2, Sox9 and Sox21 in mouse neural stem cells

Project description:Definition of genome wide binding profile of Olig2, Ascl1, Tcf3, Max, NFI, Sox2, Sox9 and Sox21 in mouse neural stem cells. Three sets of processed data files, together with a README file (README_E-MTAB-2228.docx) describing the source and content of each file, are provided as additional files to this ArrayExpress submission and can be found in https://www.ebi.ac.uk/arrayexpress/files/E-MTAB-2228 .

2014-09-19 | E-MTAB-2228 | biostudies-arrayexpress

Gene analysis of ameloblasts in Sox21KO

Project description:Tooth and hair development starts from ectodermal invaginations. However, the determination of organ-specific cell fates is poorly understood. The transcription factor Sox21 is expressed in the epithelium of developing teeth. We discovered that disruption of Sox21 caused severe enamel hypoplasia and ectopic hair formation in the gingiva in Sox21 knockout incisors. We dissected tooth germ from P1 Sox21 KO and control incisors for microarray. In particular, several markers of ameloblast maturity, i.e. amelotin (Amtn), laminin α3 (Lama3), and kallikrein-related peptidase 4 (Klk4), were included among the downregulated molecules in Sox21 KO tooth germ, whereas the expression of Mmp20 and Amel was not changed. On the other hand, numerous keratin-related genes were upregulated in the Sox21 KO tooth germ and WT skin. As in the microarray results, the expression of dental epithelial stem cell marker Sox2, as well as keratin family and hair-related genes such as Lgr5, were increased in Sox21 KO dental epithelium. Taken together, these results reflected the perturbed differentiation of ameloblasts and a cell fate change in the Sox21 KO incisors.

2020-01-01 | GSE99359 | GEO

Gene expression profiling reveals a novel regulatory role for Sox21 in mouse trophoblast stem cell differentiation.

2015-11-10 | GSE67037 | GEO

Gene expression profiling reveals a novel regulatory role for Sox21 in mouse trophoblast stem cell differentiation.

Project description:In this study we introduced Sox21 as a new regulator of trophoblast stem cell (TSC) differentiation. The transcriptome of different cell types were analyzed and compared to identify a TSC gene signature. In order to identify novel TSC specific genes, we performed genome-wide expression profiling of TSCs, embryonic stem cells, epiblast stem cells, and mouse embryo fibroblasts derived from mice of the same genetic background (129S1/SvImJ).

2015-11-10 | E-GEOD-67037 | biostudies-arrayexpress

Fate specification of neural plate border by canonical Wnt signaling and Grhl3 is crucial for neural tube closure.

Project description:During primary neurulation, the separation of a single-layered ectodermal sheet into the surface ectoderm (SE) and neural tube specifies SE and neural ectoderm (NE) cell fates. The mechanisms underlying fate specification in conjunction with neural tube closure are poorly understood. Here, by comparing expression profiles between SE and NE lineages, we observed that uncommitted progenitor cells, expressing stem cell markers, are present in the neural plate border/neural fold prior to neural tube closure. To identify what type of signaling pathways and transcriptional factors are involved in the fate specification between SE and NE cells during neurulation.

2015-04-17 | E-GEOD-67977 | biostudies-arrayexpress

Chd5 regulates a ribosome biogenesis switch controlling neural cell fate specification

Project description:Cell fate specification of neural stem/progenitor cells (NSCs) is an intricate developmental process that determines neural cell identity. While transcriptional mechanisms undoubtedly affect this process, translational mechanisms are much less understood. Here we show that deficiency of the chromatin remodeler Chromodomain Helicase DNA binding protein 5 (Chd5) causes transcriptional de-repression of multiple ribosomal subunit genes, increases protein synthesis, and expands the activated stem cell pool leading to perturbation of NSC fate. Compromised H3K27me3 in Chd5 deficient NSCs during early cell fate specification underlies the generation of excessive astrocytes at the expense of neurons at later stages of differentiation. Chd5 expression rescues these cell fate defects while simultaneously reestablishing H3K27me3, and inhibition of the H3K27me3-specific demethylase Utx restores appropriate cell fate specification in NSCs lacking Chd5. These findings define a Chd5-Utx-H3K27me3 axis pivotal in ribosome biogenesis and translation during neurogenesis, consistent with compromised CHD5 being implicated in glioma.

2018-08-22 | GSE80583 | GEO

A Transcription Factor Atlas of Directed Differentiation [10XscRNA_191108_TFv2d56]

Project description:10X single-cell RNA-seq data profiling spontaneously differentiated cells from induced neural progenitors produced by combining RFX4 overexpression and dual SMAD inhibition

2023-01-05 | GSE216457 | GEO

Switch Enhancer Elements Control Cell Fate in Human Embryonic Stem Cells (BeadChip)

Project description:A small toolkit of morphogens is used repeatedly to direct development, raising the question of how context dictates interpretation of the same cue. One example is the TGFβ pathway that in human embryonic stem cells fulfills two opposite functions: pluripotency maintenance and mesendoderm (ME) specification. Using proteomics coupled to analysis of genome occupancy, we uncover a regulatory complex comprised of transcriptional effectors of the Hippo pathway (TAZ/YAP/TEAD), the TGFβ pathway (SMAD2/3) and the pluripotency regulator OCT4 (TSO). TSO collaborates with NuRD repressor complexes to buffer pluripotency gene expression, while suppressing ME genes. Importantly, the SMAD DNA binding partner FOXH1, a major specifier of ME, is found near TSO elements and upon fate specification we show that TSO is disrupted with subsequent SMAD-FOXH1 induction of ME. These studies define switch enhancer elements and provide a framework to understand how cellular context dictates interpretation of the same morphogen signal in development. Total RNA was isolated from human embryonic stem cells (WA09) 48h after siRNA transfection (siCntr, siTAZ/YAP, siTEAD1-4)

2013-12-18 | E-GEOD-52439 | biostudies-arrayexpress

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