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The ac4C acetyltransferase Nat10 promotes RNA stability to support hematopoietic stem cell fate [acRIP-seq]

ABSTRACT: The control of gene expression program is believed to underlie hematopoietic stem cell (HSC) homeostasis. However, a comprehensive molecular understanding of the RNA level regulation is currently lacking. Here we provide evidence that the HSC-associated transcripts have longer 3’UTRs and more enriched AU-rich elements (AREs), which were recognized by Nat10. Nat10 is highly expressed in HSC and its deficiency disrupts HSC self-renewal and long-term maintenance. In contrast to current model that invoke ac4C modification to mediate downstream effects, we find Nat10 recruits ribosomes to mRNA 3’UTRs and protects them from degradation by ZFP36-CNOT RNA decay complex. Nat10 depletion leads to reduction of mRNA hail-life, and both wild-type and catalytically inactive Nat10 promote the stability of mRNA with AREs. We present a model that Nat10 regulates mRNA stability as an ARE-binding protein rather than ac4C writer in HSC, a mechanism is required for hematopoietic homeostasis, highlighting the importance of transcript-specific characteristics determining the contribution of Nat10 in HSC fate.

ORGANISM(S): Mus musculus

PROVIDER: GSE276134 | GEO | 2026/03/21

REPOSITORIES: GEO

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The ac4C acetyltransferase Nat10 promotes RNA stability to support hematopoietic stem cell fate [RNA-seq-mouse]

Project description:The control of gene expression program is believed to underlie hematopoietic stem cell (HSC) homeostasis. However, a comprehensive molecular understanding of the RNA level regulation is currently lacking. Here we provide evidence that the HSC-associated transcripts have longer 3’UTRs and more enriched AU-rich elements (AREs), which were recognized by Nat10. Nat10 is highly expressed in HSC and its deficiency disrupts HSC self-renewal and long-term maintenance. In contrast to current model that invoke ac4C modification to mediate downstream effects, we find Nat10 recruits ribosomes to mRNA 3’UTRs and protects them from degradation by ZFP36-CNOT RNA decay complex. Nat10 depletion leads to reduction of mRNA hail-life, and both wild-type and catalytically inactive Nat10 promote the stability of mRNA with AREs. We present a model that Nat10 regulates mRNA stability as an ARE-binding protein rather than ac4C writer in HSC, a mechanism is required for hematopoietic homeostasis, highlighting the importance of transcript-specific characteristics determining the contribution of Nat10 in HSC fate.

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Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are characterized by excessive triglyceride accumulation in the liver. However, due to an incomplete understanding of its pathogenesis, more efforts are still needed to identify specific and effective treatments. N4-acetylcytidine (ac4C) is a newly discovered RNA modification to regulate mRNA stability post-transcriptionally. N-acetyltransferase 10 (NAT10), the sole enzyme catalyzing mRNA acetylation, has not been fully explored in human diseases, especially in MASLD and MASH. In the current study, abundant RNA acetylation was found in lipid metabolism-related genes in the livers of leptin receptor-deficient (db/db) mice. Besides, hepatic NAT10 expression is significantly increased in multiple mouse models of MASLD and MASH. NAT10 expression is also elevated in patients with MASLD and positively correlated with clinical characteristics. Genetic NAT10 knockdown protects against diet-induced hepatic steatosis and steatohepatitis in mice, while its overexpression exacerbates steatosis. Mechanistically, NAT10 could bind to Srebp-1c mRNA to promote its stability and expression, thereby upregulating lipogenic enzymes. In addition, the translational significance of our findings is that treatment of Remodelin, an NAT10 inhibitor, could improve liver steatosis and dyslipidemia in a preclinical mouse model. Together, these findings highlight the significance of ac4C modification and NAT10 in MASLD and MASH, offering a potential therapeutic target for disease treatment.

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Project description:NAT10-catalyzed N4-acetylcytidine (ac4C) has emerged as a vital post-transcriptional modulator on the coding transcriptome by promoting mRNA stability. To explore the transcriptome-wide profile of ac4C modification, we mapped the locations of ac4C modification on wild-type (WT) hESCs and NAT10 KD hESCs by NaCNBH3-based chemical ac4C sequencing (ac4C-seq).

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