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Early anteroposterior regionalization of human neural crest is shaped by a pro-mesodermal factor

ABSTRACT: Early anteroposterior regionalization of human neural crest is shaped by a pro-mesodermal factor

PROVIDER: PRJNA763606 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15908316.fastq.gz	Fastqsanger.gz
	SRR15908317.fastq.gz	Fastqsanger.gz
	SRR15908318.fastq.gz	Fastqsanger.gz
	SRR15908319.fastq.gz	Fastqsanger.gz
	SRR15908320.fastq.gz	Fastqsanger.gz

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Early anteroposterior regionalisation of human neural crest is shaped by a pro-mesodermal factor

Project description:Early anteroposterior regionalisation of human neural crest is shaped by a pro-mesodermal factor

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Early anteroposterior regionalization of human neural crest is shaped by a pro-mesodermal factor

Project description:We employed ATAC-seq to interrogate the chromatin accessibility landscape in neuromesodermal progenitor (NMP)-like cells derived from a human embryonic stem cell (hESC) line engineered to exhibit shRNA-mediated, tetracycline (Tet)-inducible knockdown of TBXT expression. TBXT shRNA hESCs were differentiated toward NMPs following a three day treatment in the presence of WNT and FGF agonists in the presence or absence of tetracycline and +/-Tet treated samples were harvested and analysed by ATAC-seq.

2021-09-18 | GSE184227 | GEO

Early anteroposterior regionalisation of human neural crest is shaped by a pro-mesodermal factor.

Project description:The neural crest (NC) is an important multipotent embryonic cell population and its impaired specification leads to various developmental defects, often in an anteroposterior (A-P) axial level-specific manner. The mechanisms underlying the correct A-P regionalisation of human NC cells remain elusive. Recent studies have indicated that trunk NC cells, the presumed precursors of childhood tumour neuroblastoma, are derived from neuromesodermal-potent progenitors of the postcranial body. Here we employ human embryonic stem cell differentiation to define how neuromesodermal progenitor (NMP)-derived NC cells acquire a posterior axial identity. We show that TBXT, a pro-mesodermal transcription factor, mediates early posterior NC/spinal cord regionalisation together with WNT signalling effectors. This occurs by TBXT-driven chromatin remodelling via its binding in key enhancers within HOX gene clusters and other posterior regulator-associated loci. This initial posteriorisation event is succeeded by a second phase of trunk HOX gene control that marks the differentiation of NMPs toward their TBXT-negative NC/spinal cord derivatives and relies predominantly on FGF signalling. Our work reveals a previously unknown role of TBXT in influencing posterior NC fate and points to the existence of temporally discrete, cell type-dependent modes of posterior axial identity control.

| S-EPMC9536837 | biostudies-literature

Early anteroposterior regionalisation of human neural crest is shaped by a pro-mesodermal factor

Project description:Undifferentiated human embryonic stem cells (hESCs) were treated with WNT and FGF agonists for three days to generate NMP-like axial progenitors (NMPs).

2021-09-23 | GSE184622 | GEO

RARγ is required for mesodermal gene expression prior to gastrulation

Project description:The developing vertebrate embryo is exquisitely sensitive to retinoic acid (RA) concentration, particularly during anteroposterior patterning. In contrast to Nodal and Wnt signaling, RA was not previously considered to be an instructive signal in mesoderm formation during gastrulation. Here we show that RARγ is indispensable for the expression of early mesoderm markers and is, therefore, an obligatory factor in mesodermal competence and/or maintenance. We identified several novel targets up-regulated by RAR signaling in the early gastrula that are expressed in the circumblastoporal ring and linked to mesodermal development. Despite overlapping expression patterns of the RA synthetic enzyme, Aldh1a2 and the RA- degrading enzyme, Cyp26a1, RARγ1 functions as a transcriptional activator in early mesoderm development, suggesting that RA ligand is available to the embryo earlier than previously appreciated. RARγ1 is required for cellular adhesion, as revealed by spontaneous dissociation and depletion of N-CAM mRNA in animal caps harvested from RARγ1 knockdown embryos. RARγ1 knockdown obliterates somite boundaries, and causes loss of MYOD protein in the presomitic mesoderm, but ectopic, persistent expression of MYOD protein in the trunk. Thus, RARγ1 is required for stabilizing the mesodermal fate, myogenic commitment, somite boundary formation, and terminal, skeletal muscle differentiation.

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CHD3 regulates BMP signalling response during cranial neural crest cell specification

Project description:CHD3 is a component of the NuRD chromatin remodeller. Mutations in CHD3 cause Snijders Blok-Campeau Syndrome, a neurodevelopmental disorder marked by intellectual disability and craniofacial abnormalities. To unveil the role of CHD3 in craniofacial development, we differentiated CHD3-null induced pluripotent stem cells (iPSCs) into cranial neural crest cells (CNCC). We found that CHD3 expression is low in iPSCs and neuroectoderm, but it is upregulated during CNCC specification, where CHD3-containing NuRD opens the chromatin at BMP-responsive enhancers, to allow binding of DLX5 and other factors. CHD3 loss leads to repression of BMP target genes and imbalance between BMP and Wnt signalling, which ultimately results in aberrant mesodermal fate. Consequently, cranial neural crest specification fails, replaced by mesodermal identity, which can be partially rescued by titrating Wnt levels. Our findings highlight a novel role for CHD3 as pivotal regulator of BMP signalling, essential for proper neural crest specification and craniofacial development.

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Age-dependent replacement of neural-crest derived enteric neurons by a novel mesodermal lineage and its functional consequences

Project description:Age-dependent replacement of neural-crest derived enteric neurons by a novel mesodermal lineage and its functional consequences

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Snail2 controls mesodermal BMP/Wnt induction of neural crest.

Project description:The neural crest is an induced tissue that is unique to vertebrates. In the clawed frog Xenopus laevis, neural crest induction depends on signals secreted from the prospective dorsolateral mesodermal zone during gastrulation. The transcription factors Snail2 (Slug), Snail1 and Twist1 are expressed in this region. It is known that Snail2 and Twist1 are required for both mesoderm formation and neural crest induction. Using targeted blastomere injection, morpholino-based loss of function and explant studies, we show that: (1) Snail1 is also required for mesoderm and neural crest formation; (2) loss of snail1, snail2 or twist1 function in the C2/C3 lineage of 32-cell embryos blocks mesoderm formation, but neural crest is lost only in the case of snail2 loss of function; (3) snail2 mutant loss of neural crest involves mesoderm-derived secreted factors and can be rescued synergistically by bmp4 and wnt8 RNAs; and (4) loss of snail2 activity leads to changes in the RNA levels of a number of BMP and Wnt agonists and antagonists. Taken together, these results identify Snail2 as a key regulator of the signals involved in mesodermal induction of neural crest.

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