ArticleCell death and differentiation2022
NAT10 regulates mitotic cell fate by acetylating Eg5 to control bipolar spindle assembly and chromosome segregation.
Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 55 citations in OpenAlex.
- NAT10 governs development through the Xrp1-mediated stress response rather than its RNA acetylation activity.Science advances · 2026Article
- TET2 aggravates podocyte mitotic catastrophe and renal injury in diabetic nephropathy via m5C-dependent downregulation of Wee1 and activation of CDK1-cyclinB1 signaling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- DUSP12 Regulates NAT10-Mediated RNA Acetylation to Modulate DNA Repair and Therapeutic Response in Hepatocellular Carcinoma.MedComm · 2026Article
- NAT10 inhibition corrects nuclear defects in tau mutant human neurons and extends lifespan in aiScience · 2026Article
- Targeting NAT10 with Remodelin reshapes the pro-fibrotic microenvironment in renal fibrogenesisActa pharmaceutica Sinica. B · 2026Article
- The functions, mechanisms and clinical relevance of RNA and protein acetyltransferase NAT10: a comprehensive review.Cell biology and toxicology · 2026Review
- RNA acetylation modification ac4C: An emerging regulatory hub of RNA metabolism disruption in Alzheimer's disease.Molecular biology reports · 2026Review
- Review
- Multiple Regulatory Mechanisms of Post-Translational Modifications and Therapeutic Potential of Mitotic Catastrophe.International journal of molecular sciences · 2026Review
- USP1 driven mitotic dysregulation and PLK1 stabilization confer Lenvatinib resistance in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- The NAT10/acCell communication and signaling : CCS · 2026Review
- The function of NAT10-driven N4-acetylcytidine modification in cancer: novel insights and potential therapeutic targets.Cell & bioscience · 2025Review
- Pre-rRNAs control mitosis by maintaining chromosomal segregation through protecting SMC2 from AURKA-mediated phosphorylation.Cell death & disease · 2025Article
- The emerging epitranscriptomic modification acNature plants · 2025Review
- Kinesin Spindle Protein (KIF11) in Mitosis and Cancer.International journal of molecular sciences · 2025Review
- Aging increases susceptibility to liver fibrosis through enhanced NAT10-mediated ac4C modification of TGFβ1 mRNA.Genome medicine · 2025Article
- CFAP100 couples microtubule glutamylation to spindle pole integrity in keratinocytes to promote epidermal development.Nature communications · 2025Article
- Emerging role of N-acetyltransferase 10 in diseases: RNA ac4C modification and beyond.Molecular biomedicine · 2025Review
- Single-cell imaging of N4-acetylcytidine-modified RNA using fluorine metabolic labeling mediated proximity ligation assay.Nucleic acids research · 2025Article
- A critical role of NNature immunology · 2025Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell fate of mitotic cell is controlled by spindle assembly. Deficient spindle assembly results in mitotic catastrophe leading to cell death to maintain cellular homeostasis. Therefore, inducing mitotic catastrophe provides a strategy for tumor therapy. Nucleolar acetyltransferase NAT10 has been found to regulate various cellular processes to maintain cell homeostasis. Here we report that NAT10 regulates mitotic cell fate by acetylating Eg5. NAT10 depletion results in multinuclear giant cells, which is the hallmark of mitotic catastrophe. Live-cell imaging showed that knockdown of NAT10 dramatically prolongs the mitotic time and induces defective chromosome segregation including chromosome misalignment, bridge and lagging. NAT10 binds and co-localizes with Eg5 in the centrosome during mitosis. Depletion of NAT10 reduces the centrosome loading of Eg5 and impairs the poleward movement of centrosome, leading to monopolar and asymmetrical spindle formation. Furthermore, NAT10 stabilizes Eg5 through its acetyltransferase function. NAT10 acetylates Eg5 at K771 to control Eg5 stabilization. We generated K771-Ac specific antibody and showed that Eg5 K771-Ac specifically localizes in the centrosome during mitosis. Additionally, K771 acetylation is required for the motor function of Eg5. The hyper-acetylation mimic Flag-Eg5 K771Q but not Flag-Eg5 rescued the NAT10 depletion-induced defective spindle formation and mitotic catastrophe, demonstrating that NAT10 controls mitosis through acetylating Eg5 K771. Collectively, we identify Eg5 as an important substrate of NAT10 in the control of mitosis and provide K771 as an essential acetylation site in the stabilization and motor function of Eg5. Our findings reveal that targeting the NAT10-mediated Eg5 K771 acetylation provides a potential strategy for tumor therapy.
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