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Development ePress online publication date 2 Oct 2008
doi: 10.1242/dev.025361

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Research article: Development and Disease

Frs2{alpha}-deficiency in cardiac progenitors disrupts a subset of FGF signals required for outflow tract morphogenesis


Jue Zhang, Yongshun Lin, Yongyou Zhang, Yongsheng Lan, Chunhong Lin, Anne M. Moon, Robert J. Schwartz, James F. Martin, and Fen Wang*
* Author for correspondence (e-mail: fwang{at}ibt.tmc.edu)

The cardiac outflow tract (OFT) is a developmentally complex structure derived from multiple lineages and is often defective in human congenital anomalies. Although emerging evidence shows that fibroblast growth factor (FGF) is essential for OFT development, the downstream pathways mediating FGF signaling in cardiac progenitors remain poorly understood. Here, we report that FRS2{alpha} (FRS2), an adaptor protein that links FGF receptor kinases to multiple signaling pathways, mediates crucial aspects of FGF-dependent OFT development in mouse. Ablation of Frs2{alpha} in mesodermal OFT progenitor cells that originate in the second heart field (SHF) affects their expansion into the OFT myocardium, resulting in OFT misalignment and hypoplasia. Moreover, Frs2{alpha} mutants have defective endothelial-to-mesenchymal transition and neural crest cell recruitment into the OFT cushions, resulting in OFT septation defects. These results provide new insight into the signaling molecules downstream of FGF receptor tyrosine kinases in cardiac progenitors.


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