ZFIN ID: ZDB-PUB-051214-1
TBX1, a DiGeorge syndrome candidate gene, is inhibited by retinoic acid
Zhang, L., Zhong, T., Wang, Y., Jiang, Q., Song, H., and Gui, Y.
Date: 2006
Source: The International journal of developmental biology   50(1): 55-61 (Journal)
Registered Authors: Song, Houyan, Wang, Yuexiang, Zhong, Tao P.
Keywords: Tbx1, retinoic acid, zebrafish, pharyngeal arch, cardiac development
MeSH Terms:
  • Animals
  • Branchial Region/drug effects
  • Branchial Region/embryology
  • DNA-Binding Proteins/antagonists & inhibitors*
  • DNA-Binding Proteins/genetics*
  • DiGeorge Syndrome/genetics*
  • Down-Regulation/drug effects
  • Down-Regulation/genetics
  • Embryo, Nonmammalian/drug effects
  • Embryo, Nonmammalian/physiology
  • Gene Expression Regulation, Developmental*/drug effects
  • In Situ Hybridization
  • Phenotype
  • Reverse Transcriptase Polymerase Chain Reaction
  • T-Box Domain Proteins/antagonists & inhibitors
  • T-Box Domain Proteins/genetics
  • Tretinoin/pharmacology
  • Tretinoin/physiology*
  • Zebrafish/embryology
  • Zebrafish Proteins/antagonists & inhibitors*
  • Zebrafish Proteins/genetics*
PubMed: 16323078 Full text @ Int. J. Dev. Biol.
Both retinoic acid (RA) and Tbx1 are definitively indispensable for the development of the pharyngeal arches. The defects produced by a loss of Tbx1 highly resemble those induced by hyper- and hypo- RA. Based on these similarities, the effects of RA on Tbx1 expression pattern were explored during pharyngeal arch development in zebrafish. Whole-mount in situ hybridization and real-time quantitative PCR were used. Zebrafish embryos were treated with 5x10(-8)mol/L and 10(-7)mol/L RA at 12.5 hours post fertilization for 1.5 hours, respectively. Whole-mount in situ hybridization showed that Tbx1 was expressed in the cardiac region, pharyngeal arch and otic vesicle between 24 hpf and 72 hpf in zebrafish. Tbx1 expression was obviously reduced, even lost, in the pharyngeal arch and outflow tract in RA treated groups. Real-time quantitative PCR analysis showed that Tbx1 expression rose to a peak level at 36 hpf in wild type group. Repression of Tbx1 expression was most evident at 36 hpf, 24 hours after RA treatment. 10(-7 )mol/L RA caused a more severe effect on the Tbx1 expression level than 5x10(-8)mol/L RA.The results suggested that RA could produce an altered Tbx1 expression pattern in zebrafish. In addition, RA could repress Tbx1 expression in a dose-dependant manner.