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Cortex Folding by Combined Progenitor Expansion and Adhesion-Controlled Neuronal Migration

ABSTRACT: Cortex Folding by Combined Progenitor Expansion and Adhesion-Controlled Neuronal Migration

PROVIDER: PRJNA1111399 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29016700.fastq.gz	Fastqsanger.gz
	SRR29016679.fastq.gz	Fastqsanger.gz
	SRR29016680.fastq.gz	Fastqsanger.gz
	SRR29016681.fastq.gz	Fastqsanger.gz
	SRR29016682.fastq.gz	Fastqsanger.gz

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Cortex Folding by Combined Progenitor Expansion and Adhesion-Controlled Neuronal Migration

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Project description:Purpose:To gain a deeper insight into how Serpina3 regulates neurogenesis and further controling cortex folding in mice brain, RNA-sequencing (RNA-seq) was performed to analyze the genome-wide changes by TCF20 deletion at E15. Methods: Total RNA was extracted from E15 telencephalic tissue of WT and serpina3 cKI 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 WT and Serpina3 knock-in brain cortex, with a fold change ≥1.5 and p value <0.05. Gene ontology (GO) analysis showed that the up-regulated genes were enriched in the terms related to neurogenesis, neuronal specification, neural differentiation and secretion by cells. Up-regulated genes showed a significant enrichment of terms involved in up regulation of hypersensitivity and down regulation of inflammatory response. These results reflected the importance of serpina3 in cortical neurogenesis and cortex folding. Conclusions: We conclude that RNA-seq based transcriptome characterization would provide a framework for understanding how serpina3 contribute to brain cortical development.

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Project description:In order to investigate the underlying molecular mechanism of Yki-regulated tracheal progenitor migration and proliferation, genomic chromatin immunoprecipitation (ChIP-seq) was performed to identify loci bound by Yki in trachea.The peaks we observed included multiple Yki binding sites in the promoter and intronic regions of expanded (ex) and Diap1, which are well-characterized direct target genes of Yki. Other Yki targets are regulators in cell migration, cell cycle, and cell adhesion, and include hnt, which is a regulator of cell cycle in follicle cells.Yki occupancy was also pronounced in the promoter region of two heparan sulfate proteoglycans (HSPGs), Dally and Dally-like protein (Dlp) , which together with Ex and Diap1 belong to the cell migration GO cluster. Significant ChIP-seq peaks were observed in the region of N-cadherin (Ncad), a cell adhesion molecule that promotes cell migration and Matrix metalloproteinase-1 (MMP-1), a component of the extracellular matrix. Together, these results suggest that Yki activates various targets that function in cell cycle, cell migration and cell adhesion.

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