ArticleCell reports2016
Nono, a Bivalent Domain Factor, Regulates Erk Signaling and Mouse Embryonic Stem Cell Pluripotency.
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Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27citing papers in PubMed
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Essential role of NONO-HOXA1-Wnt axis in cardiomyocyte differentiation.Nature communications · 2026Article
- Review
- Paraspeckle protein NONO regulates active chromatin by allosterically stimulating NSD1.Cell reports · 2025Article
- Downregulation of NONO Suppresses Proliferation, Migration, and Invasion in Metastatic Prostate Cancer.The Prostate · 2025Article
- PRC2 primes bivalent genes for transcription induction independent of histone methyltransferase activity.Science China. Life sciences · 2024Article
- Nono induces Gadd45b to mediate DNA repair.Life science alliance · 2024Article
- The pleiotropic nature of NONO, a master regulator of essential biological pathways in cancers.Cancer gene therapy · 2024Review
- Established and Evolving Roles of the Multifunctional Non-POU Domain-Containing Octamer-Binding Protein (NonO) and Splicing Factor Proline- and Glutamine-Rich (SFPQ).Journal of developmental biology · 2024Review
- The disordered C terminus of ALKBH5 promotes phase separation and paraspeckles assembly.The Journal of biological chemistry · 2023Article
- NONO enhances mRNA processing of super-enhancer-associated GATA2 and HAND2 genes in neuroblastoma.EMBO reports · 2023Article
- A NANOG-pERK reciprocal regulatory circuit regulates Nanog autoregulation and ERK signaling dynamics.EMBO reports · 2022Article
- Condensates induced by transcription inhibition localize active chromatin to nucleoli.Molecular cell · 2022Article
- A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency.Cell reports · 2022Article
- SETMAR, a case of primate co-opted genes: towards new perspectives.Mobile DNA · 2022Review
- Article
- Transcriptional silencing of fetal hemoglobin expression by NonO.Nucleic acids research · 2021Article
- AF10 (MLLT10) prevents somatic cell reprogramming through regulation of DOT1L-mediated H3K79 methylation.Epigenetics & chromatin · 2021Article
- NONO Inhibits Lymphatic Metastasis of Bladder Cancer via Alternative Splicing of SETMAR.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Chromatin-Associated Membraneless Organelles in Regulation of Cellular Differentiation.Stem cell reports · 2020Review
- Differential Histone Distribution Patterns in Induced Asymmetrically Dividing Mouse Embryonic Stem Cells.Cell reports · 2020Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 2 countries.
Chun MaKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Violetta Karwacki-NeisiusNewborn Medicine Division, Boston Children's Hospital, Boston, MA 02115, USA; Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Haoran TangKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Wenjing LiKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Zhennan ShiKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Haolin HuKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Wenqi XuKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Zhentian WangKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Lingchun KongKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Ruitu LvKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Zheng FanKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Wenhao ZhouKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China.
Pengyuan YangDepartment of Systems Biology, Institutes of Biomedical Sciences, Fudan University, 138 Yixue Yuan Road, Shanghai 200032, China.
Feizhen WuKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Jianbo DiaoKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Li TanKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
Yujiang Geno ShiKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Division of Endocrinology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Fei LanKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China. Electronic address: fei_lan@fudan.edu.cn.
Yang ShiKey Laboratory of Birth Defects, Children's Hospital and Key Laboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai 201102, China; Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China; Newborn Medicine Division, Boston Children's Hospital, Boston, MA 02115, USA; Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: yshi@hms.harvard.edu.
Fudan University · CNChildren's Hospital of Fudan University · CNBoston Children's Hospital · USBrigham and Women's Hospital · US
Funding
Mouse Neurodevelopmental Behavior CoreU54HD090255 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI POMEROY, SCOTT LOREN · 2016 to 2020
$5.2MHistone Demethylases and Regulation of Chromatin and Transcription in EukaryotesR01CA118487 · NCI · HARVARD MEDICAL SCHOOL · PI SHI, YANG · 2006 to 2017
$3.6MNCI NIH HHS R01 CA118487NICHD NIH HHS U54 HD090255
Abstract
Nono is a component of the para-speckle, which stores and processes RNA. Mouse embryonic stem cells (mESCs) lack para-speckles, leaving the function of Nono in mESCs unclear. Here, we find that Nono functions as a chromatin regulator cooperating with Erk to regulate mESC pluripotency. We report that Nono loss results in robust self-renewing mESCs with epigenomic and transcriptomic features resembling the 2i (GSK and Erk inhibitors)-induced "ground state." Erk interacts with and is required for Nono localization to a subset of bivalent genes that have high levels of poised RNA polymerase. Nono loss compromises Erk activation and RNA polymerase poising at its target bivalent genes in undifferentiated mESCs, thus disrupting target gene activation and differentiation. These findings argue that Nono collaborates with Erk signaling to regulate the integrity of bivalent domains and mESC pluripotency.
Indexed as
MAP Kinase Signaling SystemAnimalsCell DifferentiationCell Self RenewalDNA-Binding ProteinsEnzyme ActivationEpigenesis, GeneticGene Expression ProfilingGenomeKruppel-Like Factor 4Kruppel-Like Transcription FactorsMiceMice, KnockoutMouse Embryonic Stem CellsNanog Homeobox ProteinPhosphorylationDNA-Binding ProteinsKruppel-Like Factor 4Kruppel-Like Transcription FactorsNanog Homeobox ProteinNono protein, mouseRNA-Binding Proteinsbivalent domainErkground statemESCNeat1Nonop54NRBpara-specklepluripotencyRNAPII
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