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H2AZ Orchestrates Neural Progenitor Cell Proliferation and Differentiation via Setd2-mediated H3K36me3 Modification [RNA-seq]

ABSTRACT: Purpose:To gain a deeper insight into how H2AZ regulates embryonic neurogenesis, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by H2AZ deletion at E12. Methods: Total RNA was extracted from E12 telencephalic tissue of H2AZcKO and H2AZfl/fl mice. Then total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately approximately one thousand transcripts showed differential expression between the H2AZfl/fl and H2AZcKO brain, with a fold change ≥1.5 and p value <0.05. Gene ontology (GO) analysis showed that the down-regulated genes were enriched in the terms related to transcription and cortex development, such as regulation of transcription, cerebellar cortex formation, forebrain development, and cerebellum development. Up-regulated genes showed a significant enrichment of terms involved in negative regulation of cell differentiation, neuron migration, and cognition. These results reflected the importance of H2AZ in cortical development. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding how a disruption in the H2AZ gene may contribute to cortical development.

ORGANISM(S): Mus musculus

PROVIDER: GSE99347 | GEO | 2017/05/29

SECONDARY ACCESSION(S): PRJNA388170

REPOSITORIES: GEO

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H2A.Z Regulates Astrocyte Proliferation and Differentiation via H3K56ac Modification

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2017-07-28 | GSE101939 | GEO

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Wt1 regulates proliferation and differentiation of neural progenitors during brain development

Project description:Purpose: To gain a total insight into how Wt1 regulates embryonic neurogenesis, RNA-seq was performed to compare the different expressed genes ar E13 Methods: Total RNA were extracted from E13 telencephalic tissue of Wt1fl/fl and Wt1CKO mice. Then the total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately approximately one thousand transcripts showed differential expression between the Wt1fl/fl and Wt1CKO mice brain cortex, with a fold change ≥1.5 and p value <0.05. These results indicated the importance of Wt1 in cortical development. Conclusions：RNA-seq based transcriptome characterization would provide a global understanding how Wt1 gene contribute to brain cortical development.

2019-05-24 | GSE131694 | GEO

PRDM16 orchestrates neuron-vascular communication for angiogenesis during brain development

Project description:Purpose:To gain a deeper insight into how PRDM16 regulates neuron-vascular communication for angiogenesis, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by PRDM16 deletion at E15. Methods: Total RNA was extracted from E15 telencephalic tissue of Prdm16cKO and Prdm16fl/fl mice. Then total RNA was quality controlled and quantified using an Agilent 2100 Bioanalyzer. After converting to cDNA and building library, high-throughput sequencing was performed using the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Approximately approximately one thousand transcripts showed differential expression between the Prdm16fl/fl and Prdm16cKO brain cortex, with a fold change ≥1.5 and p value <0.05. Gene ontology (GO) analysis showed that the down-regulated genes were enriched in the terms related to neurogenesis, blood vessel development and secretion by cells. Up-regulated genes showed a significant enrichment of terms involved in negative regulation of cell communication and negative regulation of angiogenesis. These results reflected the importance of PRDM16 in cortical development. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding how Prdm16 gene contribute to brain cortical development.

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H2AZ Orchestrates Neural Progenitor Cell Proliferation and Differentiation via Setd2-mediated H3K36me3 Modification [ChIP-seq]

Project description:We report the genomic characterization of H2AZ binding at E13 brain. ChIP experiment was performed with antibody against H2AZ. we generated genome-wide characterization of H2AZ occupancy and find that H2AZ was prone to bind the promoter and the intergenic regions. The genomic localization of H2AZ might reveal its essential role during early neurogenesis. Gene ontology (GO) analysis, revealing that these genes occupied by H2AZ play roles in the cellular metabolic process, DNA replication, cell cycle, and neuron development and so on. Detailed investigation of the binding profiles show that direct binding of NkX2-4 by H2AZ. This study provides a framework for the epigenetic regulation of H2AZ in embryonic neurogenesis.

2017-05-29 | GSE99348 | GEO

Chromatin immunopreciptiation of H2AZ in mouse embryonic stem cells and neural precursor cells

Project description:Elucidating how chromatin organization influences gene expression patterns and ultimately cell fate is fundamental to understanding development and disease. Histone variants have emerged as key regulators of genome function by creating specialized chromatin domains. The histone variant H2AZ plays an essential, but poorly understood function during early mammalian development. Genome-wide analysis reveals that H2AZ is enriched at a large class of developmentally important genes that are known targets of Polycomb-mediated repression in embryonic stem (ES) cells. H2AZ displays a highly defined spatial patterning that is remarkably similar to the Polycomb group (PcG) protein Suz12 in ES cells, but not in differentiated cell types. By using RNA interference, we demonstrate that H2AZ is a critical regulatory component at developmental genes in ES cells and show that localization of H2AZ and PcG proteins is interdependent at target promoters. Moreover, similarly to Suz12, H2AZ is required for lineage commitment. This study reveals a connection between H2AZ and PcG proteins in ES cells and suggests that these factors functionally interact to regulate chromatin states necessary for the proper execution of developmental gene expression programs.

2009-01-22 | E-TABM-556 | biostudies-arrayexpress

Gasdermin D deficiency affects mitochondrial dynamics and metabolic to orchestrates neurogenesis during embryonic development

Project description:Purpose: To gain futher insight into how GSDMD regulates the proliferative of neural progenitors ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortices of E13 GSDMD conditional knock out mice and littermate wild-type. Methods: Total RNA from E13 telencephalic tissue of wild-type(WT) and Gsdmdfl/fl;Nestin-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and Gsdmdfl/fl;Nestin-Cre mice brain cortex, with a fold change ≥1.5 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development and proliferation.The down-regulated genes exhibited enrichment of biological processes related to the negative regulation of cell proliferation and developmental process. These results reflected GSDMD plays a role in cortex development. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how GSDMD gene contribute to brain cortical development.

2023-11-13 | GSE247326 | GEO

H2AZ extended acidic patch is necessary for formation specialized chromatin states in ESCs [RNA-Seq]

Project description:The H2A variant H2AZ is essential for embryonic development and for proper execution of developmental gene expression programs in embryonic stem cells (ESCs). Divergent regions in H2AZ are likely key for its functional specialization, but we know little about how these differences contribute to chromatin regulation. Here, we show that the extended acidic patch, specifically the three divergent residues in the C-terminal docking domain, is necessary for lineage commitment during ESC differentiation and proper execution of gene expression programs during ESC differentiation. Surprisingly, disruption of the acidic patch domain has a distinct consequence on cellular specification compared to H2AZ depletion. This is consistent with differences in gene expression profiles of H2AZ M-bM-^@M-^Sdepleted and acidic patch (AP) mutant ESCs during early lineage commitment. Interestingly, the distinct consequence of AP mutant expression on gene regulation is coincidence with an altered destabilized chromatin state and high chromatin mobility dependent on active transcription. Collectively, our data shows that the divergent residues within the acidic patch domain are key structural determinants of H2AZ function and links chromatin structure and dynamics with gene regulation and cell fate specification. H2AZ extended acidic patch was mutated, or H2AZ was KD in mouse embryonic stem cells and RNA-Seq analysis was performed on the resulting cultures. Characterization of H2AZ-WT and -AP3-mutant binding specificities were performed by ChIP-Seq.

2013-09-23 | E-GEOD-40064 | biostudies-arrayexpress

H2AZ extended acidic patch is necessary for formation specialized chromatin states in ESCs [ChIP-Seq]

2013-09-23 | E-GEOD-40063 | biostudies-arrayexpress

H2AZ extended acidic patch is necessary for formation specialized chromatin states in ESCs [RNA-Seq]

Project description:The H2A variant H2AZ is essential for embryonic development and for proper execution of developmental gene expression programs in embryonic stem cells (ESCs). Divergent regions in H2AZ are likely key for its functional specialization, but we know little about how these differences contribute to chromatin regulation. Here, we show that the extended acidic patch, specifically the three divergent residues in the C-terminal docking domain, is necessary for lineage commitment during ESC differentiation and proper execution of gene expression programs during ESC differentiation. Surprisingly, disruption of the acidic patch domain has a distinct consequence on cellular specification compared to H2AZ depletion. This is consistent with differences in gene expression profiles of H2AZ –depleted and acidic patch (AP) mutant ESCs during early lineage commitment. Interestingly, the distinct consequence of AP mutant expression on gene regulation is coincidence with an altered destabilized chromatin state and high chromatin mobility dependent on active transcription. Collectively, our data shows that the divergent residues within the acidic patch domain are key structural determinants of H2AZ function and links chromatin structure and dynamics with gene regulation and cell fate specification.

2013-09-23 | GSE40064 | GEO

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