Deficiency of STING-signaling leads to neurogenic abnormalities and Autistic-Like Behaviors in the embryonic cortex [bulk RNA-seq]

Purpose: To gain futher insight into how STING regulates the proliferative of neural progenitors ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortices of E13 STING conditional knock out mice and littermate wild-type. Methods: Total RNA from E13 telencephalic tissue of wild-type(WT) and STINGf/f;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 STINGf/f;Nestin-Cre mice brain cortex, with a fold change =1.5 and p value <0.05.Geneontology analysis of the down or up-regulated genes showed obvious enrichment of biological processes related to brain development and cell fate commitment. These results reflected STING plays a role in cortex development. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how STING gene contribute to brain cortical development. Overall design: Total mRNA profiles of E13 wild type (WT) and STINGf/f;Nestin-Cre mice were generated by deep sequencing using Illumina HiSeq 2500.