Project description:To investigate the transcriptome changes in embryonic and postnatal mouse hearts, we performed gene expression profiling analysis using data obtained from RNA-seq of C57BL/6J mouse hearts at embryonic day 18.5 (E18.5d), postnatal 1st day (P1d) and postnatal 7th day (P7d).
Project description:We Investigate of the mice hearts from embryonic day 10.5 to postnatal week 8 and reveal developmental changes in phosphoproteome, proteome encompassing cardiogenesis and cardiac maturation.
Project description:We report the applicatin of Methylation RNA Immunoprecipitation with Next Generation Sequencing (MeRIP-seq) technology for high-throughput status of m6A methylation modifications in mouse embryonic and postnatal cerebral cortices. By data analysis, we provided the distinct status of m6A methylation between embryonic and postnatal cortices.
Project description:To gain an integrated view of the dynamic changes in gene expression during postnatal heart development at the organ level, time-series transcriptome analyses of the postnatal hearts of neonatal through adult mice (P1, P7, P14, P30, and P60) were performed using a newly developed bioinformatics pipeline. Additionally, the role of the transcription factor Sox6 in the postnatal maturation of cardiac muscle was investigated by differential transcriptome analyses between Sox6 knockout (KO) and control hearts.
Project description:Identification of the embryonic germ cell Meioc-/- transcriptome, MEIOC targets in postnatal testis, and YTHDC2 targets in postnatal testis in mouse
Project description:We report the genome-wide RNA sequencing changes to isolated retinal ganglion cells (RGCs) from immunopanned embryonic day 18 (E18) and early postnatal (P5) wildtype mouse retinas. We report the transcriptomic change associated with RGCs in a survival and regenerative state, and use gene-set enrichment analysis (GSEA) to predict the upstream transcription factors likely regulating these observed changes.
Project description:Embryos from the Dp1Tyb mouse model for Down syndrome (DS) present with congenital heart defects similar to the heart defects seen in humans with DS. We found that genetically reducing the copy number of the Dyrk1a gene (one of the genes in 3 copies in DS) from 3 to 2, normalised some of the transcriptomic changes in Dp1Tyb embryonic hearts and rescued congenital heart defects. Here we treated pregnant mice carrying Dp1Tyb and wild-type (WT) embryos with a Dyrk1a pharmacological inhibitor (Leucettinib-21 or L21) or an inactive isomer (Iso-L21) to study the effect of L21 on the transcriptome of Dp1Tyb and WT embryonic hearts.
Project description:We generated mouse heart organoids from mouse embryonic stem cells. The heart organoids showed both atrium-like and ventricle-like morphology similar to those of embryonic hearts. Therefore we performed RNA-seq analysis to compare atrial and ventricular gene expression profiles between mouse embryonic hearts and induced heart organoids.
Project description:We performed bulk RNAseq on whole hearts from E13.5 Dp3Tyb embryos and from wild-type littermates, as well as hearts from E13.5 Ts1Rhr embryos and wild-type littermates. Analysis showed the expected increased expression of the Hsa21-orthologous genes on Mmu16 that are present in 3 copies. Gene set enrichment analysis identified pathways that are altered in Dp3Tyb and Ts1Rhr hearts.