ArticleThe Journal of biological chemistry2012
Jarid2 (Jumonji, AT rich interactive domain 2) regulates NOTCH1 expression via histone modification in the developing heart.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- The Many Faces of SetDB1.Epigenomes · 2026Review
- Homozygous variant in JARID2 causes female infertility characterized by compromised blastulation efficiency.Journal of ovarian research · 2025Article
- The neurodevelopmental regulatory role and clinical value of hsa-circ-CORO1C-hsa-miR-708-3p-JARID2 + LNPEP axis in early-onset schizophrenia.Schizophrenia (Heidelberg, Germany) · 2024Article
- To Erase or Not to Erase: Non-Canonical Catalytic Functions and Non-Catalytic Functions of Members of Histone Lysine Demethylase Families.International journal of molecular sciences · 2024Review
- Cfp1 Controls Cardiomyocyte Maturation by Modifying Histone H3K4me3 of Structural, Metabolic, and Contractile Related Genes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Roles of Histone Lysine Methyltransferases in Heart Development and Disease.Journal of cardiovascular development and disease · 2023Review
- Role of Histone Deacetylases in the Pathogenesis of Salivary Gland Tumors and Therapeutic Targeting Options.International journal of molecular sciences · 2023Review
- Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1.Cell reports · 2023Article
- Molecular Cloning and Expression Responses ofGenes · 2022Article
- DNA Methylation Signature forInternational journal of molecular sciences · 2022Article
- Nuclear deformation guides chromatin reorganization in cardiac development and disease.Nature biomedical engineering · 2021Article
- Structure, Activity and Function of the SETDB1 Protein Methyltransferase.Life (Basel, Switzerland) · 2021Review
- Competition between PRC2.1 and 2.2 subcomplexes regulates PRC2 chromatin occupancy in human stem cells.Molecular cell · 2021Article
- JARID2 haploinsufficiency is associated with a clinically distinct neurodevelopmental syndrome.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- Genetic and epigenetic mechanisms in the development of congenital heart diseases.World journal of pediatric surgery · 2021Review
- Endothelial-Myocardial Angiocrine Signaling in Heart Development.Frontiers in cell and developmental biology · 2021Review
- DNA methylation patterns from peripheral blood separate coronary artery disease patients with and without heart failure.ESC heart failure · 2020Article
- Epigenetics and Mechanobiology in Heart Development and Congenital Heart Disease.Diseases (Basel, Switzerland) · 2019Review
- Myocardial-specific ablation ofThe Journal of biological chemistry · 2019Article
- JARID2 and the PRC2 complex regulate skeletal muscle differentiation through regulation of canonical Wnt signaling.Epigenetics & chromatin · 2018Article
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Authors and funding
6 authors.
Funding
Abstract
Jarid2/Jumonji, the founding member of the Jmj factor family, critically regulates various developmental processes, including cardiovascular development. The Jmj family was identified as histone demethylases, indicating epigenetic regulation by Jmj proteins. Deletion of Jarid2 in mice resulted in cardiac malformation and increased endocardial Notch1 expression during development. Although Jarid2 has been shown to occupy the Notch1 locus in the developing heart, the precise molecular role of Jarid2 remains unknown. Here we show that deletion of Jarid2 results in reduced methylation of lysine 9 on histone H3 (H3K9) at the Notch1 genomic locus in embryonic hearts. Interestingly, SETDB1, a histone H3K9 methyltransferase, was identified as a putative cofactor of Jarid2 by yeast two-hybrid screening, and the physical interaction between Jarid2 and SETDB1 was confirmed by coimmunoprecipitation experiments. Concurrently, accumulation of SETDB1 at the site of Jarid2 occupancy was significantly reduced in Jarid2 knock out (KO) hearts. Employing genome-wide approaches, putative Jarid2 target genes regulated by SETDB1 via H3K9 methylation were identified in the developing heart by ChIP-chip. These targets are involved in biological processes that, when dysregulated, could manifest in the phenotypic defects observed in Jarid2 KO mice. Our data demonstrate that Jarid2 functions as a transcriptional repressor of target genes, including Notch1, through a novel process involving the modification of H3K9 methylation via specific interaction with SETDB1 during heart development. Therefore, our study provides new mechanistic insights into epigenetic regulation by Jarid2, which will enhance our understanding of the molecular basis of other organ development and biological processes.
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