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N4-acetylcytidine of Nop2 mRNA is Required to the Transition of Morula-to-Blastocyst

ABSTRACT: N4-acetylcytidine of Nop2 mRNA is Required to the Transition of Morula-to-Blastocyst

PROVIDER: PRJNA993164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25221738_1.fastq.gz	Fastqsanger.gz
	SRR25221738_2.fastq.gz	Fastqsanger.gz
	SRR25221739_1.fastq.gz	Fastqsanger.gz
	SRR25221739_2.fastq.gz	Fastqsanger.gz

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N4-acetylcytidine of Nop2 mRNA is Required to the Transition of Morula-to-Blastocyst

Project description:N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification is crucial for mRNA stability and translation efficiency, yet the underlying function in mammalian preimplantation embryos remains unclear.

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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) modification mainly occurs on tRNA, rRNA, and mRNA, playing an important role in the expression of genetic information. However, it is still unclear whether microRNAs have undergone ac4C modification and their potential physiological and pathological functions. In this study, we identified that NAT10/THUMPD1 acetylates primary microRNAs (pri-miRNAs) with ac4C modification. Knockdown of NAT10 suppresses and augments the expression levels of mature miRNAs and pri-miRNAs, respectively. Molecular mechanism studies found that pri-miRNA ac4C promotes the processing of pri-miRNA into precursor miRNA (pre-miRNA) by enhancing the interaction of pri-miRNA and DGCR8, thereby increasing the biogenesis of mature miRNA. Knockdown of NAT10 attenuates the oncogenic characters of lung cancer cells by regulating miRNA production in cancers. Moreover, NAT10 is highly expressed in various clinical cancers and negatively correlated with poor prognosis. Thus, our results reveal that NAT10 plays a crucial role in cancer initiation and progression by modulating pri-miRNA ac4C to affect miRNA production, which would provide an attractive therapeutic strategy for cancers.

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