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Antibody-free fluorine assisted metabolic sequencing of RNA N4-acetylcytidine

ABSTRACT: Antibody-free fluorine assisted metabolic sequencing of RNA N4-acetylcytidine

PROVIDER: PRJNA983845 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24920359_1.fastq.gz	Fastqsanger.gz
	SRR24920359_2.fastq.gz	Fastqsanger.gz
	SRR24920360_1.fastq.gz	Fastqsanger.gz
	SRR24920360_2.fastq.gz	Fastqsanger.gz
	SRR24920361_1.fastq.gz	Fastqsanger.gz

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Antibody-free fluorine assisted metabolic sequencing of RNA N4-acetylcytidine

Project description:More researches have revealed that N4-acetylcytidine (ac4C) affected a variety of cellular and biological processes. In order to better understand the ac4C roles in biology and disease, we present an antibody-free, fluorine assisted metabolic sequencing method to detect RNA N4-acetylcytidine, called ‘FAM-seq’. We have successfully applied FAM-seq to profile ac4C landscapes in humans. By comparing with the classic ac4C antibody sequencing method, we demonstrated that FAM-seq is a convenient and specific method for transcriptome-wide detection of ac4C. This method holds promise to detect nascent RNA ac4C modifications.

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Project description:N4-acetylcytidine (ac4C) is an evolutionarily conserved RNA modification that is deposited on diverse RNAs by N-acetyltransferase 10 (NAT10), a protein with high biological significance for aging and cancer. Here, we performed a comprehensive survey of ac4C using metabolic labeling, sodium cyanoborohydride chemical treatment coupled to next generation sequencing (NGS) and ac4C antibody-based cell and molecular biology techniques. Our NGS analysis confirms robust ac4C modification of rRNA and specific tRNA species in a NAT10-dependent manner, but suggests low or spurious ac4C acetylation in mRNA. Analysis of RNA-seq data also revealed an induction of inflammatory responses as well as mutagenesis at transcriptionally active sites in NAT10-KO cells. This finding led us to further explore the role of NAT10 in R-loops, which have recently been shown to induce APOBEC3B-mediated mutagenesis. Our analysis revealed that R-loops are modified with ac4C in a NAT10-dependent manner. Furthermore, NAT10 restrains the levels of R-loops at a subset of differentially expressed genes in a manner dependent on its catalytic activity. Together with cellular biology data showing ac4C containing RNA in endosomal structures, we propose that increased levels of ac4C-unmodified RNAs, likely derived from R-loops, in endosomal structures induce inflammatory responses.

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