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Genome-wide association of Geminin and Zic1 during neuroectodermal cell specification

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

ORGANISM(S): Mus musculus

PROVIDER: GSE81595 | GEO | 2016/12/01

SECONDARY ACCESSION(S): PRJNA322060

REPOSITORIES: GEO

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Genome-wide association of Geminin and Zic1 during neuroectodermal cell specification

Project description:Genome-wide association of Geminin and Zic1 during neuroectodermal cell specification

| PRJNA322060 | ENA

Genome-wide chromatin binding profiles for Zic1 and Geminin during neuroectodermal cell specification

Project description:Cell intrinsic factors that control neuroectoderm specification of early embryonic cells include the nucleoprotein Geminin (Gmnn) and the Zic family of zinc finger transcription factors. Gmnn modulates chromatin state to activate neural gene expression during neural cell fate acquisition, while Gmnn deficiency in the forming neural plate disrupts transcriptional programs that control neural cell specification, neural plate patterning and neurogenesis, resulting in neural tube defects. Likewise, Zic1 over-expression promotes neural gene expression, while heterozygous deletion of Zic1/4 leads to Dandy-Walker malformation, the most common congenital cerebellar malformation. During embryonic development, Geminin and Zic1 expression is enriched in neuroectoderm from gastrula stages, with broad expression in the forming CNS during post-gastrula stages, when neural tube closure and neurogenesis are initiated. To gain a greater understanding of the molecular events that regulate neural cell specification, here we used ChIP-seq to define genome-wide chromatin binding profiles for Gmnn in embryonic stem cells (ESCs) and for Gmnn and Zic1 during specification of ESCs into neuroectoderm.

2016-12-01 | GSE77246 | GEO

Gene regulatory networks in neural cell fate acquisition from genome-wide chromatin association of Geminin and Zic1.

Project description:Neural cell fate acquisition is mediated by transcription factors expressed in nascent neuroectoderm, including Geminin and members of the Zic transcription factor family. However, regulatory networks through which this occurs are not well defined. Here, we identified Geminin-associated chromatin locations in embryonic stem cells and Geminin- and Zic1-associated locations during neural fate acquisition at a genome-wide level. We determined how Geminin deficiency affected histone acetylation at gene promoters during this process. We integrated these data to demonstrate that Geminin associates with and promotes histone acetylation at neurodevelopmental genes, while Geminin and Zic1 bind a shared gene subset. Geminin- and Zic1-associated genes exhibit embryonic nervous system-enriched expression and encode other regulators of neural development. Both Geminin and Zic1-associated peaks are enriched for Zic1 consensus binding motifs, while Zic1-bound peaks are also enriched for Sox3 motifs, suggesting co-regulatory potential. Accordingly, we found that Geminin and Zic1 could cooperatively activate the expression of several shared targets encoding transcription factors that control neurogenesis, neural plate patterning, and neuronal differentiation. We used these data to construct gene regulatory networks underlying neural fate acquisition. Establishment of this molecular program in nascent neuroectoderm directly links early neural cell fate acquisition with regulatory control of later neurodevelopment.

| S-EPMC5121602 | biostudies-literature

Geminin promoter occupancy and Geminin-dependent histone acetylation during neuroectodermal cell specification

Project description:The nucleoprotein Geminin (Gmnn) promotes neural cell fate acquisition of embryonic stem cells, while knockdown reduces the efficiency of neural gene activation. This occurs, at least in part, through Geminin’s ability to promote histone hyperacetylation at neural genes, to activate their expression. In mouse models in vivo, Geminin deficiency in the embryonic neural tube between embryonic days 8.5-10.5 also reduces the expression of genes controlling neural specification and/or differentiation, contributing to neural tube defects. To determine where Geminin binding and Gmnn-dependent acetylation occurs throughout the genome, we performed ChIP-chip analysis (these data) and ChIP-seq analysis (GSE77246) to define Geminin-bound chromatin locations in mouse embryonic stem cells (ESCs) and in ESC-derived neuroectoderm. We also performed ChIP-chip analysis of H3K9 acetylation in ESC-derived neuroectoderm, with or without Doxycycline-dependent Gmnn knockdown, to define the requirements for Geminin activity for histone acetylation of promoters during neural fate specification.

2016-12-01 | GSE81450 | GEO

Dynamic analysis of gene expression and genome wide transcription factor binding during lineage-specification of multipotent progenitors

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-10-15 | E-GEOD-49991 | biostudies-arrayexpress

Dynamic analysis of gene expression and genome wide transcription factor binding during lineage-specification of multipotent progenitors

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

2013-10-15 | GSE49991 | GEO

Geminin regulates the transcriptional and epigenetic status of neuronal fate promoting genes during mammalian neurogenesis

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-06 | E-GEOD-39673 | biostudies-arrayexpress

A genome-wide relay of signalling-responsive enhancers drives hematopoietic specification

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

2022-12-09 | GSE198775 | GEO

Zic1 and Zic4 regulate zebrafish roof plate specification and hindbrain ventricle morphogenesis.

Project description:During development, the lumen of the neural tube develops into a system of brain cavities or ventricles, which play important roles in normal CNS function. We have established that the formation of the hindbrain (4th) ventricle in zebrafish is dependent upon the pleiotropic functions of the genes implicated in human Dandy Walker Malformation, Zic1 and Zic4. Using morpholino knockdown we show that zebrafish Zic1 and Zic4 are required for normal morphogenesis of the 4th ventricle. In Zic1 and/or Zic4 morphants the ventricle does not open properly, but remains completely or partially fused from the level of rhombomere (r) 2 towards the posterior. In the absence of Zic function early hindbrain regionalization and neural crest development remain unaffected, but dorsal hindbrain progenitor cell proliferation is significantly reduced. Importantly, we find that Zic1 and Zic4 are required for development of the dorsal roof plate. In Zic morphants expression of roof plate markers, including lmx1b.1 and lmx1b.2, is disrupted. We further demonstrate that zebrafish Lmx1b function is required for both hindbrain roof plate development and 4th ventricle morphogenesis, confirming that roof plate formation is a critical component of ventricle development. Finally, we show that dorsal rhombomere boundary signaling centers depend on Zic1 and Zic4 function and on roof plate signals, and provide evidence that these boundary signals are also required for ventricle morphogenesis. In summary, we conclude that Zic1 and Zic4 control zebrafish 4th ventricle morphogenesis by regulating multiple mechanisms including cell proliferation and fate specification in the dorsal hindbrain.

| S-EPMC2268115 | biostudies-literature

Cell-cell interaction modulates neuroectodermal specification of embryonic stem cells.

Project description:The controlled differentiation of embryonic stem (ES) cells is of utmost interest to their clinical, biotechnological, and basic science use. Many investigators have combinatorially assessed the role of specific soluble factors and extracellular matrices in guiding ES cell fate, yet the interaction between neighboring cells in these heterogeneous cultures has been poorly defined due to a lack of conventional tools to specifically uncouple these variables. Herein, we explored the role of cell-cell interactions during neuroectodermal specification of ES cells using a microfabricated cell pair array. We tracked differentiation events in situ, using an ES cell line expressing green fluorescent protein (GFP) under the regulation of the Sox1 gene promoter, an early marker of neuroectodermal germ cell commitment in the adult forebrain. We observed that a previously specified Sox1-GFP+ cell could induce the specification of an undifferentiated ES cell. This induction was modulated by the two cells being in contact and was dependent on the age of previously specified cell prior to coculture. A screen of candidate cell adhesion molecules revealed that the expression of connexin (Cx)-43 correlated with the age-dependent effect of cell contact in cell pair experiments. ES cells deficient in Cx-43 showed aberrant neuroectodermal specification and lineage commitment, highlighting the importance of gap junctional signaling in the development of this germ layer. Moreover, this study demonstrates the integration of microscale culture techniques to explore the biology of ES cells and gain insight into relevant developmental processes otherwise undefined due to bulk culture methods.

| S-EPMC2448393 | biostudies-literature

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