ArticlePloS one2009
Nkx2.7 and Nkx2.5 function redundantly and are required for cardiac morphogenesis of zebrafish embryos.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 59 citations in OpenAlex.
- Nkx2.7 is a conserved regulator of craniofacial development.Nature communications · 2025Article
- Zebrafish as a Versatile Model for Cardiovascular Research: Peering into the Heart of the Matter.Cells · 2025Review
- The Interaction Between theInternational journal of molecular sciences · 2025Article
- Exposure to nitrate and nitrite disrupts cardiovascular development through estrogen receptor in zebrafish embryos and larvae.Fish physiology and biochemistry · 2024Article
- AnFrontiers in cardiovascular medicine · 2022Article
- An eIF3a gene mutation dysregulates myocardium growth with left ventricular noncompaction via the p-ERK1/2 pathway.Genes & diseases · 2021Article
- Fish-Ing for Enhancers in the Heart.International journal of molecular sciences · 2021Review
- Mending a broken heart:Disease models & mechanisms · 2021Review
- Gon4l/Udu regulates cardiomyocyte proliferation and maintenance of ventricular chamber identity during zebrafish development.Developmental biology · 2020Article
- sox9b is required in cardiomyocytes for cardiac morphogenesis and function.Scientific reports · 2018Article
- Nkx genes establish second heart field cardiomyocyte progenitors at the arterial pole and pattern the venous pole through Isl1 repression.Development (Cambridge, England) · 2018Article
- Article
- Nkx2.5 regulates endothelin converting enzyme-1 during pharyngeal arch patterning.Genesis (New York, N.Y. : 2000) · 2017Article
- Novel adverse outcome pathways revealed by chemical genetics in a developing marine fish.eLife · 2017Article
- An early requirement for nkx2.5 ensures the first and second heart field ventricular identity and cardiac function into adulthood.Developmental biology · 2015Article
- Mesodermal Nkx2.5 is necessary and sufficient for early second heart field development.Developmental biology · 2014Article
- Nkx genes are essential for maintenance of ventricular identity.Development (Cambridge, England) · 2013Article
- Genetic abnormalities in FOXP1 are associated with congenital heart defects.Human mutation · 2013Article
- Proliferation of embryonic cardiomyocytes in zebrafish requires the sodium channel scn5Lab.Genesis (New York, N.Y. : 2000) · 2013Article
- DiGeorge syndrome gene tbx1 functions through wnt11r to regulate heart looping and differentiation.PloS one · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNkx2.7 is the tinman-related gene, as well as orthologs of Nkx2.5 and Nkx-2.3. Nkx2.7 and Nkx2.5 express in zebrafish heart fields of lateral plate mesoderm. The temporal and spatial expression patterns of Nkx2.7 are similar to those of Nkx2.5, but their functions during cardiogenesis remain unclear. METHODOLOGY/PRINCIPAL
findingsHere, Nkx2.7 is demonstrated to compensate for Nkx2.5 loss of function and play a predominant role in the lateral development of the heart, including normal cardiac looping and chamber formation. Knocking down Nkx2.5 showed that heart development was normal from 24 to 72 hpf. However, when knocking down either Nkx2.7 or Nkx2.5 together with Nkx2.7, it appeared that the heart failed to undergo looping and showed defective chambers, although embryos developed normally before the early heart tube stage. Decreased ventricular myocardium proliferation and defective myocardial differentiation appeared to result from late-stage up-regulation of bmp4, versican, tbx5 and tbx20, which were all expressed normally in hearts at an early stage. We also found that tbx5 and tbx20 were modulated by Nkx2.7 through the heart maturation stage because an inducible overexpression of Nkx2.7 in the heart caused down-regulation of tbx5 and tbx20. Although heart defects were induced by overexpression of an injection of 150-pg Nkx2.5 or 5-pg Nkx2.7 mRNA, either Nkx2.5 or Nkx2.7 mRNA rescued the defects induced by Nkx2.7-morpholino(MO) and Nkx2.5-MO with Nkx2.7-MO. CONCLUSIONS AND SIGNIFICANCE: Therefore, we conclude that redundant activities of Nkx2.5 and Nkx2.7 are required for cardiac morphogenesis, but that Nkx2.7 plays a more critical function, specifically indicated by the gain-of-function and loss-of- function experiments where Nkx2.7 is observed to regulate the expressions of tbx5 and tbx20 through the maturation stage.
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