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First published online 2 October 2008
doi: 10.1242/dev.025437

Development 135, 3599-3610 (2008)
Published by The Company of Biologists 2008
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An FGF autocrine loop initiated in second heart field mesoderm regulates morphogenesis at the arterial pole of the heart

Eon Joo Park1,*, Yusuke Watanabe2,*, Graham Smyth3, Sachiko Miyagawa-Tomita4, Erik Meyers3, John Klingensmith3, Todd Camenisch5, Margaret Buckingham2 and Anne M. Moon1,6,7,{dagger}

1 Department of Neurobiology and Anatomy, University of Utah, Salt Lake City, UT 84112, USA.
2 Department of Developmental Biology, CNRS URA 2578, Pasteur Institute, Paris 75015, France.
3 Department of Cell Biology, Duke University, Durham, NC 27710, USA.
4 Department of Pediatric Cardiology, Tokyo Women's Medical University, Tokyo 162-8666, Japan.
5 Department of Pharmacology and Toxicology, University of Arizona, Tuscon, AZ 85721, USA.
6 Department of Pediatrics, University of Utah, Salt Lake City, UT 84112, USA.
7 Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, UT 84112, USA.

{dagger} Author for correspondence (e-mail: anne.moon{at}genetics.utah.edu)

Accepted 4 September 2008

In order to understand how secreted signals regulate complex morphogenetic events, it is crucial to identify their cellular targets. By conditional inactivation of Fgfr1 and Fgfr2 and overexpression of the FGF antagonist sprouty 2 in different cell types, we have dissected the role of FGF signaling during heart outflow tract development in mouse. Contrary to expectation, cardiac neural crest and endothelial cells are not primary paracrine targets. FGF signaling within second heart field mesoderm is required for remodeling of the outflow tract: when disrupted, outflow myocardium fails to produce extracellular matrix and TGFβ and BMP signals essential for endothelial cell transformation and invasion of cardiac neural crest. We conclude that an autocrine regulatory loop, initiated by the reception of FGF signals by the mesoderm, regulates correct morphogenesis at the arterial pole of the heart. These findings provide new insight into how FGF signaling regulates context-dependent cellular responses during development.

Key words: FGF, Heart development, Outflow tract, Second heart field, Autocrine signaling, Epithelial-mesenchymal transformation, Mouse


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