ArticleeLife2016
Loss of the transcription factor Meis1 prevents sympathetic neurons target-field innervation and increases susceptibility to sudden cardiac death.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
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- Spatiotemporal dynamics of the developing zebrafish enteric nervous system at the whole-organ level.Developmental cell · 2025Article
- RLS-associated MEIS transcription factors control distinct processes in human neural stem cells.Scientific reports · 2024Article
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- In Vivo Dissection of Chamber-Selective Enhancers Reveals Estrogen-Related Receptor as a Regulator of Ventricular Cardiomyocyte Identity.Circulation · 2023Article
- The autism-associated Meis2 gene is necessary for cardiac baroreflex regulation in mice.Scientific reports · 2022Article
- Identification of PAX6 and NFAT4 as the Transcriptional Regulators of the Long Noncoding RNA Mrhl in Neuronal Progenitors.Molecular and cellular biology · 2022Article
- Transcription factor Meis1 act as a new regulator of ischemic arrhythmias in mice.Journal of advanced research · 2022Article
- Identification of cortical interneuron cell markers in mouse embryos based on machine learning analysis of single-cell transcriptomics.Frontiers in neuroscience · 2022Article
- Restless legs syndrome.Nature reviews. Disease primers · 2021Review
- Genome-Wide Analysis Identifies an Essential Human TBX3 Pacemaker Enhancer.Circulation research · 2020Article
- Role of defective calcium regulation in cardiorespiratory dysfunction in Huntington's disease.JCI insight · 2020Article
- Homeobox gene Meis1 modulates cardiovascular regeneration.Seminars in cell & developmental biology · 2020Review
- Blood pressure profile and endothelial function in restless legs syndrome.Scientific reports · 2019Article
- Caenorhabditis elegans and its applicability to studies on restless legs syndrome.Advances in pharmacology (San Diego, Calif.) · 2019Review
- DIVERSITY in binding, regulation, and evolution revealed from high-throughput ChIP.PLoS computational biology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although cardio-vascular incidents and sudden cardiac death (SCD) are among the leading causes of premature death in the general population, the origins remain unidentified in many cases. Genome-wide association studies have identified Meis1 as a risk factor for SCD. We report that Meis1 inactivation in the mouse neural crest leads to an altered sympatho-vagal regulation of cardiac rhythmicity in adults characterized by a chronotropic incompetence and cardiac conduction defects, thus increasing the susceptibility to SCD. We demonstrated that Meis1 is a major regulator of sympathetic target-field innervation and that Meis1 deficient sympathetic neurons die by apoptosis from early embryonic stages to perinatal stages. In addition, we showed that Meis1 regulates the transcription of key molecules necessary for the endosomal machinery. Accordingly, the traffic of Rab5(+) endosomes is severely altered in Meis1-inactivated sympathetic neurons. These results suggest that Meis1 interacts with various trophic factors signaling pathways during postmitotic neurons differentiation.
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