GSE119564
Zfp217 orchestrates m6A mRNA methylation and gene expression to promote adipogenic differentiation
We performed RNA sequencing (RNA-seq) and m6A methylated RNA immunoprecipitation sequencing (MeRIP-seq) in control and Zfp217 knockout 3T3L1 cells with MDI treatment for 0d and 2d Loss-of-function study demonstrates that Zfp217 deficiency impaired adipogenesis together with a global increase of m6A modification in 3T3L1cells. To gain an overview of the global role of Zfp217 in adipogenesis, we performed RNA sequencing (RNA-seq) in control and Zfp217 knockout 3T3L1 cells with MDI treatment for 0d and 2d and identified 12,188 and 11,566 different expressed genes (DEG) for 0d and 2d, respectively. Next, to elucidate the mechanism by which Zfp217 regulates m6A restriction, m6A methylated RNA immunoprecipitation sequencing (MeRIP-seq) was used to analyze the m6A mRNA methylation in control and Zfp217 knockout 3T3L1 cells with MDI treatment for 0d and 2d, and identified 3149 and 294 of m6A peaks experienced an increase in m6A RNA modification after Zfp217 depletion, respectively. Overall design: Examination of gene expressive levels, m6A enrichment levels, in control and Zfp217 knockout 3T3L1 cells with MDI treatment for 0d and 2d