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N-acetyltransferase NAT10 Controls Cell Fates

ABSTRACT: Here, we show that NAT10 is an essential regulator of cellular plasticity, and its catalyzed mRNA cytidine acetylation represents a new layer of epitranscriptomic modulation.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Embryonic Stem Cell

SUBMITTER: Zhensheng Hu

LAB HEAD: Saiyong Zhu

PROVIDER: PXD036888 | Pride | 2023-11-14

REPOSITORIES: Pride

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			Action	DRS
	2022040801_HZS_KO_REP1_20220509224108.raw	Raw
	2022040801_HZS_KO_REP2_20220510005942.raw	Raw
	2022040801_HZS_KO_REP3_20220510031815.raw	Raw
	2022040801_HZS_WT_REP1_20220509154536.raw	Raw
	2022040801_HZS_WT_REP2_20220509180404.raw	Raw

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Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [RNA-seq]

Project description:Increased differentiation or activity of osteoclasts is the key pathogenic factor of postmenopausal osteoporosis (PMOP). N4-acetylcytidine (ac4C) modification, catalyzed by Nat10, is a novel post-transcriptional mRNA modification related to many diseases. However, its impact on regulating osteoclast activation in PMOP remains uncertain. Here, we initially observed that Nat10-mediated ac4C positively correlates with osteoclast differentiation of monocytes and low bone mass in PMOP. The specific knockout of Nat10 in monocytes and remodelin, a Nat10 inhibitor, alleviates ovariectomized (OVX)-induced bone loss by downregulating osteoclast differentiation. Mechanistically, epitranscriptomic analyses reveal that the nuclear factor of activated T cells cytoplasmic 1 (Nfatc1) is the key downstream target of ac4C modification during osteoclast differentiation. Subsequently, translatomic results demonstrate that Nat10-mediated ac4C enhances the translation efficiency of Nfatc1, thereby inducing Nfatc1 expression and consequent osteoclast maturation. Cumulatively, these findings reveal the promotive role of Nat10 in osteoclast differentiation and PMOP from a novel field of RNA modifications and suggest that Nat10 can be a target of epigenetic therapy for preventing bone loss in PMOP.

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Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [Ribo-seq]

Project description:Increased differentiation or activity of osteoclasts is the key pathogenic factor of postmenopausal osteoporosis (PMOP). N4‐acetylcytidine (ac4C) modification, catalyzed by Nat10, is a novel post-transcriptional mRNA modification related to many diseases. However, its impact on regulating osteoclast activation in PMOP remains uncertain. Here, we initially observed that Nat10-mediated ac4C positively correlates with osteoclast differentiation of monocytes and low bone mass in PMOP. The specific knockout of Nat10 in monocytes and remodelin, a Nat10 inhibitor, alleviates ovariectomized (OVX)-induced bone loss by downregulating osteoclast differentiation. Mechanistically, epitranscriptomic analyses reveal that the nuclear factor of activated T cells cytoplasmic 1 (Nfatc1) is the key downstream target of ac4C modification during osteoclast differentiation. Subsequently, translatomic results demonstrate that Nat10-mediated ac4C enhances the translation efficiency of Nfatc1, thereby inducing Nfatc1 expression and consequent osteoclast maturation. Cumulatively, these findings reveal the promotive role of Nat10 in osteoclast differentiation and PMOP from a novel field of RNA modifications and suggest that Nat10 can be a target of epigenetic therapy for preventing bone loss in PMOP.

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N-acetyltransferase NAT10 Controls Cell Fates via RNA Cytidine Acetylation

Project description:N-acetyltransferase NAT10 Controls Cell Fates via RNA Cytidine Acetylation

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ac4C RIP-seq analysis of AGS cells upon NAT10 knockout.

Project description:N4-acetylcytidine (ac4C), a conserved chemical modification in eukaryotic prokaryotes that is catalyzed by the N-acetyltransferase 10 (NAT10) enzyme, plays a crucial role in promoting mRNA stability and translation. However, the biological function and mechanisms of NAT10-mediated ac4C in human cancer were poorly defined. In order to investigate the regulatory mechanism of NAT10 in gastric cancer, we performed ac4C RIP-seq(acRIP-seq) analysis in AGS cells with NAT10 knockout compared with control in two repeats.

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NAT10 depletion suppresses fatty acid metabolism in MCF7 breast cancer cells

Project description:NAT10 is an RNA cytidine transferase known to add acetyl group on RNA transcripts thereby promoting translational efficiency. It was reported that NAT10 regulates epithelial to mesenchymal transition (EMT), DNA damage, and cell proliferation in cancers. However, weather NAT10 regulates other crucial pathways is unknown. In our study we conducted gene expression profiling analysis using data obtained from RNA-seq of MCF7 NAT10 KO and scramble control. High throughput sequencing revealed fatty acid metabolism as the top enriched pathway with fatty acid metabolic genes such ELOVL6, ACSL1, ACSL3, ACSL4, ACADSB, and ACAT1 were found to be differentially down-regulated. Overall our results revealed NAT10 depletion suppresses fatty acid metabolism in MCF7.

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RNA Cytidine Acetyltransferase NAT10 Maintains T Cell Pathogenicity in Inflammatory Bowel Disease

Project description:The enzyme N-acetyltransferase 10 (NAT10), known as the exclusive catalyst for N4-acetylcytidine (ac4C) modification, has been associated with various cellular processes, including tRNA acetylation, 18S rRNA biogenesis, mRNA stability, and translational efficiency. Despite extensive investigation into its molecular mechanisms in vitro, the physiological function of NAT10 under normal conditions has remained largely undefined. In this study, we found that the deficiency of NAT10 led to a disruption of T cell development at steady state, and identified a pivotal role for NAT10 in preserving the pathogenicity of naïve CD4+ T cells to induce adoptive transfer colitis. Mechanistically, the lack of NAT10 triggers the diminished stability of the anti-apoptotic gene Bag3, initiating a cascade of events that includes the upregulation of apoptosis-related genes and an accelerated rate of apoptosis in T cells. Our findings reveal a previously unrecognized role of the NAT10-ac4C-Bag3 axis in maintaining T cell homeostasis in vivo.

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N-acetyltransferase NAT10 Controls Cell Fates via RNA Cytidine Acetylation

Project description: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.

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