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ZFIN ID: ZDB-PUB-110502-3
Heart chamber size in zebrafish is regulated redundantly by duplicated tbx2 genes
Sedletcaia, A., and Evans, T.
Date: 2011
Source: Developmental dynamics : an official publication of the American Association of Anatomists 240(6): 1548-1557 (Journal)
Registered Authors: Evans, Todd
Keywords: cardiogenesis, T-box, cardiomyocytes, nppa, ndrg4
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Cell Proliferation
  • Embryo, Nonmammalian
  • Gene Dosage/physiology
  • Gene Duplication*/physiology
  • Gene Expression Regulation, Developmental
  • Heart/embryology*
  • Heart/growth & development
  • Heart Defects, Congenital/embryology
  • Heart Defects, Congenital/genetics
  • Heart Defects, Congenital/veterinary
  • Myocytes, Cardiac/metabolism
  • Myocytes, Cardiac/physiology
  • Organ Size/genetics
  • T-Box Domain Proteins/genetics*
  • T-Box Domain Proteins/metabolism
  • T-Box Domain Proteins/physiology
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Zebrafish/growth & development
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
  • Zebrafish Proteins/physiology
PubMed: 21448936 Full text @ Dev. Dyn.
The Tbx2 transcription factor is implicated in growth control based on its association with human cancers. In the heart, Tbx2 represses cardiac differentiation to mediate development of the atrioventricular canal (AVC). The zebrafish genome retains two tbx2 genes, and both are required for formation of the AVC. Here, we show that both genes are also expressed earlier in the primitive heart tube, and we describe a previously unrecognized role for Tbx2 in promoting proliferation of presumptive myocardium at the heart tube stage. In contrast to single knockdowns, depletion of both gene products causes chamber defects, resulting in an expanded atrium and a smaller ventricle, associated with decreased proliferation of ventricular cardiomyocytes. The phenotype correlates with changes in the expression for known cardiac growth factors. Therefore, in zebrafish, two tbx2 genes are functionally redundant for regulating chamber development, while each gene is required independently for development of the AVC.