GSE210504
N-acetyltransferase NAT10 Controls Cell Fates via RNA Cytidine Acetylation
We show that NAT10-ac4C axis significantly regulates cell fates. To identify the molecular mechanisms of NAT10-ac4C-ANP32B axis in cell-fate transitions, we construct shNAT10 and shANP32B hESCs. acRIP-seq of shCTR and shNAT10 hESCs. We profiled ATAC-seq in shCTR, shNAT10, and shANP32B hESCs. We profiled H3K4me3 and H3K27me3 modifications and the binding of ANP32B by CUT&Tag in shCTR and shNAT10 hESCs. Overall design: RNA-seq to find transcriptional differences between shCTR and shNAT10 hESCs and also as the input of acRIP-seq.acRIP-seq to identify acetylation targets. ATAC-seq to observe the changes in chromatin accessibility with NAT10 or ANP32B suppression. H3K4me3 and H3K27me3 CUT&Tag to examine their changes after NAT10 suppression. ANP32B CUT&Tag to profile the genome-wide chromatin binding of ANP32B. RNA-seq to find transcriptional differences between shCTR and shANP32B cells. We performed ATAC-seq to explore the regulation of ANP32B on chromatin accessibility in cell-fate transitions.