ArticleJCI insight2022
Prdm6 controls heart development by regulating neural crest cell differentiation and migration.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- The Roles of the PRDM Family in the Neuro-Motor System.Biomolecules · 2026Review
- The HOX code of human adult fibroblasts reflects their ectomesenchymal or mesodermal origin.Histochemistry and cell biology · 2025Article
- Transcriptional regulation of the postnatal cardiac conduction system heterogeneity.Nature communications · 2024Article
- Update in genetic and epigenetic causes of hypertension.Cellular and molecular life sciences : CMLS · 2024Review
- Clinical and Genetic Correlation in Neurocristopathies: Bridging a Precision Medicine Gap.Journal of clinical medicine · 2024Review
- Unsupervised ensemble-based phenotyping enhances discoverability of genes related to left-ventricular morphology.Nature machine intelligence · 2024Article
- The Roles of Histone Lysine Methyltransferases in Heart Development and Disease.Journal of cardiovascular development and disease · 2023Review
- Prdm6 drives ductus arteriosus closure by promoting ductus arteriosus smooth muscle cell identity and contractility.JCI insight · 2023Article
- A systems biology approach identifies the role of dysregulated PRDM6 in the development of hypertension.The Journal of clinical investigation · 2023Article
- Impaired Human Cardiac Cell Development due to NOTCH1 Deficiency.Circulation research · 2023Article
- ScRNA-seq and spatial transcriptomics: exploring the occurrence and treatment of coronary-related diseases starting from development.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 4 countries.
Funding
Abstract
The molecular mechanisms that drive the acquisition of distinct neural crest cell (NCC) fates is still poorly understood. Here, we identified Prdm6 as an epigenetic modifier that temporally and spatially regulates the expression of NCC specifiers and determines the fate of a subset of migrating cardiac NCCs (CNCCs). Using transcriptomic analysis and genetic and fate mapping approaches in transgenic mice, we showed that disruption of Prdm6 was associated with impaired CNCC differentiation, delamination, and migration and led to patent ductus arteriosus (DA) and ventricular noncompaction. Bulk and single-cell RNA-Seq analyses of the DA and CNCCs identified Prdm6 as a regulator of a network of CNCC specification genes, including Wnt1, Tfap2b, and Sox9. Loss of Prdm6 in CNCCs diminished its expression in the pre-epithelial-mesenchymal transition (pre-EMT) cluster, resulting in the retention of NCCs in the dorsal neural tube. This defect was associated with diminished H4K20 monomethylation and G1-S progression and augmented Wnt1 transcript levels in pre-EMT and neural tube clusters, which we showed was the major driver of the impaired CNCC migration. Altogether, these findings revealed Prdm6 as a key regulator of CNCC differentiation and migration and identified Prdm6 and its regulated network as potential targets for the treatment of congenital heart diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.