Project description:Tthis study is aimed to explore how C1qbp deficiency affects the mRNA expressing profiling during the differentiation stage of CD8+ T cells.Naïve WT and C1qbp KO P14 cells and transferred WT and C1qbp KO P14 cells sorted from the spleen of donor mice on day 3, 5, 7 post-infection with LCMV Armstrong were collected and treated for RNA-seq. RNA-Seq analysis revealed transcriptomic changes between WT and C1qbp KO CD8+ T cells. Naïve WT and C1qbp KO CD8+ T cells showed similar gene expressing profiling. On day 3, 5, 7 post-infection with LCMV Armstrong, WT and C1qbp KO CD8+ T cells showed 341, 1,164 and 437 differentially expressed genes respectively.
Project description:This study is aimed to explore whether C1qbp deficiency affects the DNA methylation status during the differentiation stage of CD8+ T cells. Transferred WT and C1qbp KO P14 cells sorted from the spleen of donor mice on day 5 post-infection with LCMV Armstrong were collected. Genomic DNA was isolated for mRRBS. mRRBS analysis provided evidence of DNA methylation changes between WT and C1qbp KO CD8+ T cells. Our study have shown that, on day 5 post-infection with LCMV Armstrong, C1qbp KO CD8+ T cells have increased level of Global DNA methylation. Moreover, C1qbp KO CD8+ T cells show hegher DNA methylation at some effector cells-signature genes.
Project description:DNMT3a is a de novo DNA methyltransferase expressed robustly after T cell activation that regulates plasticity of CD4+ T cell cytokine expression. Here we show that DNMT3a is critical for directing early CD8+ T cell effector and memory fate decisions. While effector function of DNMT3a knockout T cells is normal, they develop more memory precursor and fewer terminal effector cells in a T cell intrinsic manner compared to wild-type animals. Rather than increasing plasticity of differentiated effector CD8+ T cells, loss of DNMT3a biases differentiation of early effector cells into memory precursor cells. This is attributed in part to ineffective repression of Tcf1 expression in knockout T cells, as DNMT3a localizes to the Tcf7 promoter and catalyzes its de novo methylation in early effector WT CD8+ T cells. This data identifies DNMT3a as a crucial regulator of CD8+ early effector cell differentiation and effector versus memory fate decisions. Examination of global genomic DNA methylation by MBD-seq in naïve CD8 T cells and CD8 T cells 8 days post Vaccinia-Ova infection, comparing OT1 TCR-Tg CD8 T cells isolated from WT and T cell conditional DNMT3a KO mice.
Project description:This study is aimed to explore whether C1qbp deficiency affects the epigenetic modification during the differentiation stage of CD8+ T cells. Transferred WT and C1qbp KO P14 cells sorted from the spleen of donor mice on day 5 post-infection with LCMV Armstrong were collected and treated for ATAC-seq. ATAC-Seq analysis provided sufficient but not necessary evidence of epigenetic changes between WT and C1qbp KO CD8+ T cells. Our study have shown that, on day 5 post-infection with LCMV Armstrong, even WT and C1qbp KO CD8+ T cells have different mRNA expressing profiling, the ATAC-seq shows slight changes in chromatin accessibility of indicated genes.
Project description:This study is aimed to Investigate whether C1qbp deficiency affects the histone modification during the differentiation stage of CD8+ T cells. Transferred WT and C1qbp KO P14 cells sorted from the spleen of donor mice on day 5 post-infection with LCMV Armstrong were collected and treated for CUT-tag. CUT-tag-Seq analysis provided evidence of histone modification changes between WT and C1qbp KO CD8+ T cells. Our study shows that on day 5 post-infection with LCMV Armstrong, along with mRNA expressing profiling, the CUT-tag-seq exhibits obvious changes in H3K27me3 and H3K27Ac modification of indicated genes of WT and C1qbp KO CD8+ T cells.