Fgf15 is required for proper morphogenesis of the mouse cardiac outflow tract

Joshua W. Vincentz, John R. McWhirter, Cornelis Murre, Antonio Baldini, Yasuhide Furuta

Research output: Contribution to journalArticlepeer-review

Abstract

Evidence in animal models indicates that signaling networks functioning in the developing pharyngeal arches regulate stereotyped processes critical for proper development of the aortic arch and cardiac outflow tract. Here, we describe the phenotype of mice lacking fibrobiast growth factor 15 (Fgf15), which encodes a secreted signaling molecule expressed within the developing pharyngeal arches. Homozygous Fgf15 mutants present heart defects consistent with malalignment of the aorta and pulmonary trunk. These defects correlate with early morphological defects of the outflow tract due to aberrant behavior of the cardiac neural crest. We demonstrate that Fgf15 expression within the pharyngeal arches is unaltered by a loss of Tbx1, a key regulator of pharyngeal arch development implicated in DiGeorge syndrome. In addition, Fgf15 and Tbx1 do not interact genetically, suggesting that Fgf15 operates through a pathway independent of Tbx1. These studies reveal a novel role of Fgf15 during development of the cardiac outflow tract.

Original languageEnglish
Pages (from-to)192-201
Number of pages10
JournalGenesis
Volume41
Issue number4
DOIs
Publication statusPublished - Apr 2005

Keywords

  • Congenital heart disease
  • Digeorge syndrome
  • Fgf15
  • Outflow tract
  • Pharyngeal arch
  • Ventricular septal defect

ASJC Scopus subject areas

  • Genetics

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