Project description:YTHDF2 displays extensive-expression patterns during oocyte maturation and its deficiency causes female infertility in mice. However, its specific mechanism of regulation remains elusive due to the absence of suitable in vitro models. Female germline stem cells (FGSCs) possess the capacity for self-renewal and differentiation into oocytes to support reproduction. The successful establishment of a line of FGSCs provides a platform for scientific research on female fertility and oogenesis. To understand how YTHDF2 exerts its regulatory effects on FGSCs, we conducted RNA-seq assay in WT and Ythdf2-KO FGSCs and aimed to identified YTHDF2-responsive genes.
Project description:YTHDF2 displays extensive-expression patterns during oocyte maturation and its deficiency causes female infertility in mice. However, its specific mechanism of regulation remains elusive due to the absence of suitable in vitro models. FGSCs possess the capacity for self-renewal and differentiation into oocytes to support reproduction. The successful establishment of a line of FGSCs provides a platform for scientific research on female fertility and oogenesis. To understand how YTHDF2 exerts its regulatory effects on FGSCs, we conducted MeRIP-seq assay in FGSCs and aimed to identified YTHDF2 target transcripts.
Project description:SUMOylation affects many aspects of target proteins such as activity, stability, localization and protein-protein interactions. We have found that SUMOylation of YTHDF2 increased its binding activity with m6A-RNAs by using different experimental approaches. To confiremd this conclusion,the analysis of RIP-seq, MeRIP-seq and RNA-seq in H1299-shYTHDF2 cells re-expressing YTHDF2-WT and YTHDF2-K571R was performed. MeRIP+RIP targets showed lower binding affinities in the mutant YTHDF2-K571R when compared with YTHDF2-WT. Compared to the control group, the binding capacities of YTHDF2 to RIP targets in treated group with either 2-D08 or GA were decreased, especially to MeRIP+RIP targets. Moreover, SUMOylated YTHDF2 promoted m6A-RNAs degradation. Combined analysis of RNA-seq, RIP-seq and MeRIP-seq showed that the mRNA levels were up-regulated in shYTHDF2 stable cells re-expressing YTHDF2-K571R compared with those in re-expressing YTHDF2-WT.
Project description:liquid chromatographytandem-mass spectrometry (LC-MS) and proteomic analysis were conducted to analyze the differential expression proteins (DEPs) in WT and SCRN1 KO cells
Project description:YTHDF2 is overexpressed in a broad spectrum of human acute myeloid leukemias (AML). To study the role of YTHDF2 in leukemia, total RNA from Ythdf2CKO (n=4) and Ythdf2CTL (n=4) leukemic stem cells were used for Affymetrix global gene expression analysis.
Project description:mRNAseq and proteomic data set of one week old WT (Chop wt/wt CkmmCre wt/wt Dars2 fl/fl), Chop KO (Chop ko/ko CkmmCre wt/wt Dars2 fl/fl), Dars2 KO (Chop wt/wt CkmmCre tg/wt Dars2 fl/fl) and DKO (Chop ko/ko CkmmCre tg/wt Dars2 fl/fl) mice
Project description:We found that the experssion of STAT5A was upregulated when the YTHDF2 was knocked down. To identify the function of STAT5A protein as a Transcription factor in YTHDF2 kockdown(KD) and wildtype(WT) cells in Multiple Myeloma. CHIP-seq was conducted to analyze changes in related signaling pathways and gene expression in Multiple Myeloma cells when YTHDF2 was knocked down.