GSE159595
C3G regulates STAT3, ERK, and adhesion signaling, and is essential for differentiation of mouse embryonic stem cells
Purpose: Here we report the differential gene expression profile between WT and C3G knock out E14Tg2a cells. The cells were grown in equel seeding density in GMEM  Serum +LIF media. RNA was isolated after 48 hr and sequenced Methods:  C3G knock out E14Tg2a mouse ES cells were made by CrisprCAS9 mediated knock out strategy. RNA was collected using Trizol method from WT and knock out clone 48 hr after seeding in equel density in a 6 well plate, precoated with gelatin. Results: Using an optimized data analysis workflow, we mapped about 75 million sequence reads per sample to the mouse genome (build mm10) and identified 5797 genes were differentially expressed with adjusted p-value < 0.05(significant) between the WT and C3G-/-.  Approximately 17% of the genes showed differential expression between the WT and C3g-/- ESCs, with a fold change =1.5 and p value <0.05. Biological pathways and gene ontology enrichment analysis of differentially expressed genes reveals that C3G is  required  to maintain adhesion of ES cells and for differentiation of mouse ES cells. Conclusions: The study revealed the first transcriptome profile of C3G gene knock out in E14Tg2a mouse embryoinic tem cells. In our study we found that C3G acts as a mediaator of differentiation by activatingERK and integrin signaling and supressing STAT3 and other pluripotency factors like ESRRB and KLF4. Overall design: Examination of differential gene expression between WT and C3G knock out E14Tg2a mouse embryonic stem cells.