ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2012
Transactivation in Drosophila of human enhancers by human transcription factors involved in congenital heart diseases.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- A systematic review of fetal genes as biomarkers of cardiac hypertrophy in rodent models of diabetes.PloS one · 2014Pooled it
- Single-Cell Multi-Omics Reveal Gene Regulatory Mechanisms Underlying Cardiac Embryonic Development.Genes · 2026Review
- SomaticExperimental and therapeutic medicine · 2024Article
- Porous, Ventricular Extracellular Matrix-Derived Foams as a Platform for Cardiac Cell Culture.BioResearch open access · 2015Article
- Ndae1 expression and regulation in Drosophila embryos.PloS one · 2014Article
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Authors and funding
5 authors at 2 institutions in 4 countries.
Funding
Abstract
backgroundThe human transcription factors (TFs) GATA4, NKX2.5 and TBX5 form part of the core network necessary to build a human heart and are involved in Congenital Heart Diseases (CHDs). The human natriuretic peptide precursor A (NPPA) and α-myosin heavy chain 6 (MYH6) genes are downstream effectors involved in cardiogenesis that have been demonstrated to be in vitro targets of such TFs.
resultsTo study the interactions between these human TFs and their target enhancers in vivo, we overexpressed them in the whole Drosophila cardiac tube using the UAS/GAL4 system. We observed that all three TFs up-regulate their natural target enhancers in Drosophila and cause developmental defects when overexpressed in eyes and wings.
conclusionsA strong potential of the present model might be the development of combinatorial and mutational assays to study the interactions between human TFs and their natural target promoters, which are not easily undertaken in tissue culture cells because of the variability in transfection efficiency, especially when multiple constructs are used. Thus, this novel system could be used to determine in vivo the genetic nature of the human mutant forms of these TFs, setting up a powerful tool to unravel the molecular genetic mechanisms that lead to CHDs.
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