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T-box genes and cardiac development.

Kenneth Ryan1, Alvin J Chin

  • 1Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Joseph Stokes Jr. Research Institute, Division of Cardiology, Abramson Research Center, Philadelphia, Pennsylvania, USA.

Birth Defects Research. Part C, Embryo Today : Reviews
|May 29, 2003
PubMed
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T-box genes are ancient and crucial for development. Mutations in TBX1 and TBX5 cause human disorders, highlighting their conserved role in cardiovascular development across species.

Area of Science:

  • Developmental Biology
  • Genetics
  • Evolutionary Biology

Background:

  • T-box genes represent an evolutionarily ancient gene family with essential roles in metazoan gastrulation and organogenesis.
  • The T-box gene family is diverse, with varying numbers of genes across species, including eight in Drosophila melanogaster, 22 in Caenorhabditis elegans, and at least 18 in mammals.

Purpose of the Study:

  • To review the current understanding of T-box gene contributions to cardiovascular morphogenesis.
  • To highlight the growing evidence for conserved roles of T-box genes in heart development.

Main Methods:

  • Utilized a range of cytological, developmental, molecular, and genetic methodologies.
  • Reviewed findings from loss-of-function models in various organisms.

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Main Results:

  • Mutations in TBX1 and TBX5 are linked to human disorders (DiGeorge/velocardiofacial syndrome, Holt-Oram syndrome) with cardiovascular phenotypes.
  • T-box genes show conserved expression domains in cardiac and pharyngeal arch tissues during vertebrate embryogenesis.
  • Tbx5 loss-of-function models in mice and zebrafish phenocopy Holt-Oram syndrome, and T-box gene expression in Drosophila cardioblasts suggests fundamental roles in cardiovascular pattern formation.

Conclusions:

  • T-box genes play fundamental and conserved roles in cardiovascular development.
  • Further research into T-box genes is warranted to understand their contribution to cardiovascular morphogenesis.