Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA309845 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3126050.fastq.gz | Fastqsanger.gz | |||
| SRR3126051.fastq.gz | Fastqsanger.gz | |||
| SRR3126052.fastq.gz | Fastqsanger.gz | |||
| SRR3126053.fastq.gz | Fastqsanger.gz | |||
| SRR3126054.fastq.gz | Fastqsanger.gz |
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Project description:Genome-wide association of Geminin and Zic1 during neuroectodermal cell specification
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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
Project description:Geminin promoter occupancy and Geminin-dependent histone acetylation during neuroectodermal cell specification
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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
Project description:To better understand the role of Geminin during germ layer specification, we bred floxed Geminin mice to Mox2-Cre mice. Mutants (fl/fl; cre/o) had spinal neural tube defects with complete penetrance. We obtained neural tube and paraxial tissue by laser capture microdissection and analyzed total RNA by microarray.
2014-09-30 | GSE42052 | GEO
Project description:To better understand the role of Geminin during germ layer specification, we bred floxed Geminin mice to Mox2-Cre mice. Mutants (fl/fl; cre/o) had spinal neural tube defects with complete penetrance. We obtained neural tube and paraxial tissue by laser capture microdissection and analyzed total RNA by microarray. Spinal neural tube and paraxial tissue were obtained separately by laser capture microdissection from wild-type and mutant E10.5 embryos. There were 2 replicates of each sample.
2014-09-30 | E-GEOD-42052 | biostudies-arrayexpress
Project description:Transcriptional targets of neurogenin (Ngnr1) were identified by over-expression of an inducible form of neurogenin in Xenopus ectodermal explants. The effects of co-expressing the nucleoprotein geminin on Ngnr1-dependent target gene transactivation were defined. Regulating the transition from lineage-restricted progenitors to terminally differentiated cells is a central aspect of nervous system development. Here, we investigated the role of the nucleoprotein geminin in regulating neurogenesis at a mechanistic level during both Xenopus primary neurogenesis and mammalian neuronal differentiation in vitro. The latter work utilized both neural cells derived from embryonic stem and embryonal carcinoma cells in vitro and neural stem cells from mouse forebrain. In all of these contexts, geminin antagonized the ability of neural bHLH transcription factors to activate transcriptional programs promoting neurogenesis. Furthermore, geminin promoted a bivalent chromatin state, characterized by the presence of both activating and repressive histone modifications, at genes encoding transcription factors that promote neurogenesis. This epigenetic state restrains the expression of genes that regulate commitment of undifferentiated stem and neuronal precursor cells to neuronal lineages. Geminin is highly expressed in undifferentiated neuronal precursor cells but is downregulated prior to differentiation. Therefore, these data support a model whereby geminin promotes the neuronal precursor cell state by modulating both the epigenetic status and expression of genes encoding neurogenesis-promoting factors. Additional developmental signals acting in these cells can then control their transition toward terminal neuronal or glial differentiation during mammalian neurogenesis. A dexamethasone-inducible (GR ligand binding domain fused) form of Xenopus neurogenin-related 1, NgnrGR, was over-expressed in Xenopus embryonic ectodermal explants, in the presence or absence of over-expressed geminin. Induction of Ngnr1 activity was used to define direct targets as previously described (EMBO J. 26(24): 5093-5108). The ability of geminin to suppress Ngnr1-dependent transactivation of its target gene programs was determined.
2012-12-06 | E-GEOD-39658 | biostudies-arrayexpress
Project description:Formation of the complex vertebrate nervous system begins when pluripotent cells of the early embryo are directed to acquire a neural fate. Although cell intrinsic controls play an important role in this process, the molecular nature of this regulation is not well defined. Here we assessed the role for Geminin, a nuclear protein expressed in embryonic cells, in neural fate acquisition from mouse embryonic stem (ES) cells. While Geminin knockdown does not affect the ability of ES cells to maintain or exit pluripotency, we found that it significantly impairs their ability to acquire a neural fate. Conversely, Geminin overexpression promotes neural gene expression, even in the presence of growth factor signaling that antagonizes neural transcriptional responses. These data demonstrate that Geminin’s activity contributes to mammalian neural cell fate acquisition. We investigated the mechanistic basis of this phenomenon and found that Geminin maintains a hyperacetylated and open chromatin conformation at neural genes. Interestingly, recombinant Geminin protein also rapidly alters chromatin acetylation and accessibility even when Geminin is combined with nuclear extract and chromatin in vitro. These findings define a novel activity for Geminin in regulation of chromatin structure. Together, these data support a role for Geminin as a cell intrinsic regulator of neural fate acquisition that promotes expression of neural genes by regulating chromatin accessibility and histone acetylation. Mouse embryonic stem cells were differentiated for two days in N2B27 medium, with or without Doxycycline-inducible shRNAmir knockdown of Geminin and compared by microarray. Three independent experiments were conducted, using two different mouse embryonic stem cell lines for Doxycycline-inducible knockdown of Geminin. The two ES lines express unique shRNAmir sequences targeting Geminin (shRNAmir #9 and #11) to control for off-target effects.
2011-03-18 | E-GEOD-25737 | biostudies-arrayexpress
Project description:Formation of the complex vertebrate nervous system begins when pluripotent cells of the early embryo are directed to acquire a neural fate. Although cell intrinsic controls play an important role in this process, the molecular nature of this regulation is not well defined. Here we assessed the role for Geminin, a nuclear protein expressed in embryonic cells, in neural fate acquisition from mouse embryonic stem (ES) cells. While Geminin knockdown does not affect the ability of ES cells to maintain or exit pluripotency, we found that it significantly impairs their ability to acquire a neural fate. Conversely, Geminin overexpression promotes neural gene expression, even in the presence of growth factor signaling that antagonizes neural transcriptional responses. These data demonstrate that Geminin’s activity contributes to mammalian neural cell fate acquisition. We investigated the mechanistic basis of this phenomenon and found that Geminin maintains a hyperacetylated and open chromatin conformation at neural genes. Interestingly, recombinant Geminin protein also rapidly alters chromatin acetylation and accessibility even when Geminin is combined with nuclear extract and chromatin in vitro. These findings define a novel activity for Geminin in regulation of chromatin structure. Together, these data support a role for Geminin as a cell intrinsic regulator of neural fate acquisition that promotes expression of neural genes by regulating chromatin accessibility and histone acetylation.
2011-03-18 | GSE25737 | GEO
Project description:Dynamic analysis of gene expression and genome wide transcription factor binding during lineage-specification of multipotent progenitors [HP]
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