GSE99347
H2AZ Orchestrates Neural Progenitor Cell Proliferation and Differentiation via Setd2-mediated H3K36me3 Modification [RNA-seq]
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. Overall design: Total RNA was extracted from E12 telencephalic tissue of H2AZcKO and H2AZfl/fl mice and generated by deep sequencing, in triplicate, using Illumina HiSeq 2500.