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NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [Ribo-seq]

ABSTRACT: We use Ribo-seq to report the most comprehensive survey to date of mRNA translation in human embryonic stem cells (hESCs), neuroepithelial progenitors cells(NEP) and mesendoderm cells(ME)

ORGANISM(S): Homo sapiens

PROVIDER: GSE225051 | GEO | 2025/11/30

REPOSITORIES: GEO

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NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [acRIP-seq]

Project description:We use acRIP-seq to report the most comprehensive survey to date of mRNA in human embryonic stem cells (hESCs), neuroepithelial progenitors cells (NEP) and mesendoderm cells (ME)

2025-11-30 | GSE225049 | GEO

NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-11-30 | GSE225052 | GEO

NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [RNA-seq]

Project description:The expression profile data was obtained by RNA-Seq data.

2025-11-30 | GSE225050 | GEO

NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [Ribo-seq]

Project description:NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [Ribo-seq]

| PRJNA934557 | ENA

NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency

Project description:NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency

| PRJNA933615 | ENA

NAT10-mediated ac<sup>4</sup>C modification promotes ectoderm differentiation of human embryonic stem cells via acetylating NR2F1 mRNA.

Project description:Cell fate determination in mammalian development is complex and precisely controlled and accumulating evidence indicates that epigenetic mechanisms are crucially involved. N4-acetylcytidine (ac4C) is a recently identified modification of messenger RNA (mRNA); however, its functions are still elusive in mammalian. Here, we show that N-acetyltransferase 10 (NAT10)-mediated ac4C modification promotes ectoderm differentiation of human embryonic stem cells (hESCs) by acetylating nuclear receptor subfamily 2 group F member 1 (NR2F1) mRNA to enhance translation efficiency (TE). Acetylated RNA immunoprecipitation sequencing (acRIP-seq) revealed that levels of ac4C modification were higher in ectodermal neuroepithelial progenitor (NEP) cells than in hESCs or mesoendoderm cells. In addition, integrated analysis of acRIP-seq and ribosome profiling sequencing revealed that NAT10 catalysed ac4C modification to improve TE in NEP cells. RIP-qRT-PCR analysis identified an interaction between NAT10 and NR2F1 mRNA in NEP cells and NR2F1 accelerated the nucleus-to-cytoplasm translocation of yes-associated protein 1, which contributed to ectodermal differentiation of hESCs. Collectively, these findings point out the novel regulatory role of ac4C modification in the early ectodermal differentiation of hESCs and will provide a new strategy for the treatment of neuroectodermal defects diseases.

| S-EPMC10984107 | biostudies-literature

NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [RNA-seq]

Project description:NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [RNA-seq]

| PRJNA934558 | ENA

NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [acRIP-seq]

Project description:NAT10-mediated ac4C modification promotes neuroectoderm specification of human embryonic stem cells via acetylating NR2F1 mRNA to enhance translation efficiency [acRIP-seq]

| PRJNA934559 | ENA

NAT10 promotes cell proliferation by acetylating <i>CEP170</i> mRNA to enhance translation efficiency in multiple myeloma.

Project description:Multiple myeloma (MM) is still an incurable hematologic malignancy, which is eagerly to the discovery of novel therapeutic targets and methods. N-acetyltransferase 10 (NAT10) is the first reported regulator of mRNA acetylation that is activated in many cancers. However, the function of NAT10 in MM remains unclear. We found significant upregulation of NAT10 in MM patients compared to normal plasma cells, which was also highly correlated with MM poor outcome. Further enforced NAT10 expression promoted MM growth in vitro and in vivo, while knockdown of NAT10 reversed those effects. The correlation analysis of acetylated RNA immunoprecipitation sequencing (acRIP-seq) and ribosome profiling sequencing (Ribo-seq) combined with RIP-PCR tests identified centrosomal protein 170 (CEP170) as an important downstream target of NAT10. Interfering CEP170 expression in NAT10-OE cells attenuated the acceleration of cellular growth caused by elevated NAT10. Moreover, CEP170 overexpression promoted cellular proliferation and chromosomal instability (CIN) in MM. Intriguingly, remodelin, a selective NAT10 inhibitor, suppressed MM cellular growth, induced cellular apoptosis in vitro and prolonged the survival of 5TMM3VT mice in vivo. Collectively, our data indicate that NAT10 acetylates CEP1 70 mRNA to enhance CEP170 translation efficiency, which suggests that NAT10 may serve as a promising therapeutic target in MM.

| S-EPMC9366180 | biostudies-literature

NAT10 regulates p53 activation through acetylating p53 at K120 and ubiquitinating Mdm2.

Project description:As a genome guardian, p53 maintains genome stability by arresting cells for damage repair or inducing cell apoptosis to eliminate the damaged cells in stress response. Several nucleolar proteins stabilize p53 by interfering Mdm2-p53 interaction upon cellular stress, while other mechanisms by which nucleolar proteins activate p53 remain to be determined. Here, we identify NAT10 as a novel regulator for p53 activation. NAT10 acetylates p53 at K120 and stabilizes p53 by counteracting Mdm2 action. In addition, NAT10 promotes Mdm2 degradation with its intrinsic E3 ligase activity. After DNA damage, NAT10 translocates to nucleoplasm and activates p53-mediated cell cycle control and apoptosis. Finally, NAT10 inhibits cell proliferation and expression of NAT10 decreases in human colorectal carcinomas. Thus, our data demonstrate that NAT10 plays a critical role in p53 activation via acetylating p53 and counteracting Mdm2 action, providing a novel pathway by which nucleolar protein activates p53 as a cellular stress sensor.

| S-EPMC4772976 | biostudies-literature

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