Project description:SETD2 is the specific methyltransferase of H3K36me3, while METTL14 is a critical subunit of the m6A methyltransferase complex. To evaluate the effect of SETD2 and METTL14 on translation, we conducted robosome profiling in SETD2 and METTL14 knockdown and control HepG2 cells. Our RNA ribosome profiling revealed that depletion of SETD2 and METTL14 resulted in a global reduction in RNA translation and the changes of translation efficiency were correlated between SETD2 and METTL14 knockdown cells.
Project description:To evaluate the effect of SETD2 and METTL14 on mRNA stability, we conducted RNA-seq in SETD2 or METTL14 knockdown HepG2 cells as well as control cells with or without actinomycin D treatment. Our RNA stability profiling revealed that depletion of SETD2 and METTL14 resulted in global reduction of RNA stability, and the changes were correlated between SETD2 and METTL14 knockdown cells.
Project description:Setd2 is the specific methyltransferase of H3K36me3. To obtain Setd2-dependent landscape of H3K36me3 in mouse genome, we used mouse embryonic stem cells (mESCs) model with doxycycline (Dox)-induced Setd2 knockdown, and performed ChIP sequencing in mESCs with or without Dox treatment.
Project description:SETD2 is the specific methyltransferase of H3K36me3, while METTL3, METTL14 and WTAP are the components of m6A methyltransferase complex. To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 and METTL3, METTL14 or WTAP knockdown HepG2 cells, and found depletion of H3K36me3 by SETD2 silencing globally reduced m6A in human transcriptome. What’s more, most of the SETD2-dependent hypomethylation sites also responded to knockdown of METTL3, METTL14, or WTAP.
Project description:Setd2 is the specific methyltransferase of H3K36me3. To understand the global effect of H3K36me3 on m6A modification, we used mouse embryonic stem cells (mESCs) model with doxycycline (Dox)-induced Setd2 knockdown, and performed m6A-IP followed by sequencing in mESCs with or without Dox treatment. We found that depletion of H3K36me3 by Setd2 silencing globally reduced m6A in mouse transcriptome.
Project description:To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 knockdown and control HepG2 cells by miCLIP-seq, and found the depletion of H3K36me3 by SETD2 silencing globally reduced m6A in the human transcriptome.
Project description:SETD2 is the specific methyltransferase of H3K36me3. To obtain SETD2-dependent landscape of H3K36me3 in human genome, we performed ChIP sequencing in SETD2 silenced and control HepG2 cells.
