ArticleDevelopmental biology2007
Gata5 and Gata6 are functionally redundant in zebrafish for specification of cardiomyocytes.
Article in Developmental biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
42 citing papers in PubMed, 82 citations in OpenAlex.
- Zebrafish as a Versatile Model for Cardiovascular Research: Peering into the Heart of the Matter.Cells · 2025Review
- An animal model recapitulates human hepatic diseases associated withProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Gata6 functions in zebrafish endoderm to regulate late differentiating arterial pole cardiogenesis.Development (Cambridge, England) · 2024Article
- Nascent transcription reveals regulatory changes in extremophile fishes inhabiting hydrogen sulfide-rich environments.Proceedings. Biological sciences · 2024Article
- Endocardium gives rise to blood cells in zebrafish embryos.Cell reports · 2024Article
- Article
- A novel causative functional mutation in GATA6 gene is responsible for familial dilated cardiomyopathy as supported by in silico functional analysis.Scientific reports · 2022Article
- GATA4/5/6 family transcription factors are conserved determinants of cardiac versus pharyngeal mesoderm fate.Science advances · 2022Article
- Neuron navigator 3 (NAV3) is required for heart development in zebrafish.Fish physiology and biochemistry · 2022Article
- Modeling Human Cardiac Arrhythmias: Insights from Zebrafish.Journal of cardiovascular development and disease · 2022Review
- From Stripes to a Beating Heart: Early Cardiac Development in Zebrafish.Journal of cardiovascular development and disease · 2021Review
- Specificity, redundancy and dosage thresholds amongBiology open · 2020Article
- Article
- Discovering human transcription factor physical interactions with genetic variants, novel DNA motifs, and repetitive elements using enhanced yeast one-hybrid assays.Genome research · 2019Article
- Dynamics of cardiomyocyte transcriptome and chromatin landscape demarcates key events of heart development.Genome research · 2019Article
- Heart enhancers with deeply conserved regulatory activity are established early in zebrafish development.Nature communications · 2018Article
- Genome-wide transcriptomics analysis identifies sox7 and sox18 as specifically regulated by gata4 in cardiomyogenesis.Developmental biology · 2018Article
- LITTLE FISH, BIG DATA: ZEBRAFISH AS A MODEL FOR CARDIOVASCULAR AND METABOLIC DISEASE.Physiological reviews · 2017Review
- Myocardial plasticity: cardiac development, regeneration and disease.Current opinion in genetics & development · 2016Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
An outstanding problem in vertebrate development has been to define the genetic program that specifies the cardiomyocyte lineage. It has been a challenge to define the transcription factors that control specification, since candidate gene knockouts typically cause rather complex morphogenetic defects. In contrast, Drosophila genetics identified single transcription factors that are essential for specification of cardiomyocytes from uncommitted mesoderm. For those vertebrate orthologs, it has been considered that paralogous family members might compensate for the loss-of-function of individual genes. However, this hypothesis had not been formally tested. In zebrafish, defects in gata5 can lead to a loss of myocardial tissue, but most embryos depleted for any single vertebrate Gata4/5/6 transcription factor develop a cardiac morphogenetic defect, and cardiomyocytes are specified and differentiate. Here we show that in zebrafish the gata5 and gata6 genes are redundant for specification of cardiomyocytes. Embryos depleted of these two gene products are heartless. Restoring either gene product is sufficient to rescue cardiomyocyte specification. In contrast, embryos depleted of Gata4 and Gata6, or Gata4 and Gata5, develop defective heart tubes. Our study identifies a specific pair of vertebrate transcription factor paralogs that is essential for cardiomyocyte specification.
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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.