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SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Xenopus laevis

PROVIDER: GSE252617 | GEO | 2024/06/26

REPOSITORIES: GEO

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SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression [ChIP-seq]

Project description:Here we investigate a functional role for SoxB1 transcription factors, Sox2 and Sox3, on the transient embryonic cell population, the neural plate border. We find through gain/loss-of-function studies necessary for neural plate border cells to become neural crest cells. and genomics experiments (ChIP-seq and RNA-seq) that SoxB1 transcription factors directly promote neural plate border formation. and that down-regulation of SoxB1 expression is

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SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression [RNA-seq]

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SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression

Project description:SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression

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SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression [RNA-seq]

Project description:SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression [RNA-seq]

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SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression [ChIP-seq]

Project description:SoxB1 transcription factors are essential for intiating and maintaining neural plate border gene expression [ChIP-seq]

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A transition from SoxB1 to SoxE transcription factors is essential for progression from pluripotent blastula cells to neural crest cells.

Project description:The neural crest is a stem cell population unique to vertebrate embryos that gives rise to derivatives from multiple embryonic germ layers. The molecular underpinnings of potency that govern neural crest potential are highly conserved with that of pluripotent blastula stem cells, suggesting that neural crest cells may have evolved through retention of aspects of the pluripotency gene regulatory network (GRN). A striking difference in the regulatory factors utilized in pluripotent blastula cells and neural crest cells is the deployment of different sub-families of Sox transcription factors; SoxB1 factors play central roles in the pluripotency of naïve blastula and ES cells, whereas neural crest cells require SoxE function. Here we explore the shared and distinct activities of these factors to shed light on the role that this molecular hand-off of Sox factor activity plays in the genesis of neural crest and the lineages derived from it. Our findings provide evidence that SoxB1 and SoxE factors have both overlapping and distinct activities in regulating pluripotency and lineage restriction in the embryo. We hypothesize that SoxE factors may transiently replace SoxB1 factors to control pluripotency in neural crest cells, and then poise these cells to contribute to glial, chondrogenic and melanocyte lineages at stages when SoxB1 factors promote neuronal progenitor formation.

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RNA Expression profiling of human induced Neural Plate Border Stem Cells, Neural Plate Border Stem Cell progeny and biological controls

Project description:We describe a so far uncharacterized, embryonic and self-renewing Neural Plate Border Stem Cell (NBSC) population with the capacity to differentiate into central nervous and neural crest lineages. NBSCs can be obtained by neural transcription factor-mediated reprogramming (BRN2, SOX2, KLF4, and ZIC3) of human adult dermal fibroblasts and peripheral blood cells (induced Neural Plate Border Stem Cells, iNBSCs) or by directed differentiation from human induced pluripotent stem cells (NBSCs). Moreover, human (i)NBSCs share molecular and functional features with an endogenous NBSC population isolated from neural folds of E8.5 mouse embryos. Upon differentiation, iNBSCs give rise to either (1) radial glia-type stem cells, dopaminergic and serotonergic neurons, motoneurons, astrocytes, and oligodendrocytes or (2) cells from the neural crest lineage. Here we provide array-based expression data of (i)NBSCs and CNS- and neural crest progeny derived thereof. The former comprise radial glia-type stem cells, while the latter are neural crest and mesenchymal stem cell-like cells. The data provided reveal that (i)NBSCs can be directed into defined neural lineages and that iNBSCs pass through successive developmental stages. These data support the notion that it is possible to reprogram human adult cells into expandable, multipotent NBSCs that define a novel embryonic neural stem cell population in human and mouse.

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Critical Role of Runx Transcription Factors in Maintaining Epididymal Epithelial Differentiation

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

2024-05-02 | GSE236105 | GEO

Znf703 is a novel RA target in the neural plate border.

Project description:Znf703 is an RAR- and Wnt-inducible transcription factor that exhibits a complex expression pattern in the developing embryo: Znf703 mRNA is found in the early circumblastoporal ring, then later throughout the neural plate and its border, and subsequently in the mid/hindbrain and somites. We show that Znf703 has a different and separable function in early mesoderm versus neural crest and placode development. Independent of its early knockdown phenotype on Gdf3 and Wnt8, Znf703 disrupts patterning of distinct neural crest migratory streams normally delineated by Sox10, Twist, and Foxd3 and inhibits otocyst formation and otic expression of Sox10 and Eya1. Furthermore, Znf703 promotes massive overgrowth of SOX2+ cells, disrupting the SoxB1 balance at the neural plate border. Despite prominent expression in other neural plate border-derived cranial and sensory domains, Znf703 is selectively absent from the otocyst, suggesting that Znf703 must be specifically cleared or down-regulated for proper otic development. We show that mutation of the putative Groucho-repression domain does not ameliorate Znf703 effects on mesoderm, neural crest, and placodes. We instead provide evidence that Znf703 requires the Buttonhead domain for transcriptional repression.

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The b-HLH transcription factor Hes3 participates in neural plate border formation by interfering with Wnt/β-catenin signaling.

Project description:Hes3 belongs to the Hes basic helix-loop-helix family of transcriptional repressors that play central roles in maintaining progenitor cells and regulating binary cell fate decisions in the embryo. During Xenopus laevis development, hes3 is expressed in the embryonic ectoderm in a horseshoe shape domain at the edge of the developing neural pate. Hes3 mis-expression at early neurula stage blocks neural crest (snai2, sox8, sox9 and sox10) and cranial placode (six1 and dmrta1) gene expression, and promotes neural plate (sox2 and sox3) fate. At tailbud stage, these embryos exhibited a massive up-regulation of both sox8 and sox10 expression, associated with an increase in genes important for melanocytes differentiation (mitf and dct). Using a hormone inducible construct we show that Hes3 does not induce a pigment cell differentiation program de novo, rather it maintains progenitor cells in an undifferentiated state, and as Hes3 expression subsides overtime these cells adopt a pigment cell fate. We demonstrate that mechanistically Hes3 mediates its activity through inhibition of Wnt/β-catenin signaling, a molecular pathway critical for neural crest specification and pigment cell lineage differentiation. We propose that Hes3 at the edge of the neural plate spatially restricts the response to mesoderm-derived Wnt ligands, thereby contributing to the establishment of sharp boundaries of gene expression at the neural plate border.

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