|
|
|
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
First published online 2 October 2008
doi: 10.1242/dev.025437
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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.
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
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati 
Twitter What's this?
Related articles in Development:
This article has been cited by other articles:
|
|
 |
|
  K. Sugiura, Y.-Q. Su, Q. Li, K. Wigglesworth, M. M. Matzuk, and J. J. Eppig Fibroblast Growth Factors and Epidermal Growth Factor Cooperate with Oocyte-Derived Members of the TGFbeta Superfamily to Regulate Spry2 mRNA Levels in Mouse Cumulus Cells Biol Reprod, November 1, 2009; 81(5): 833 - 841. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. D. Combs and K. E. Yutzey Heart Valve Development: Regulatory Networks in Development and Disease Circ. Res., August 28, 2009; 105(5): 408 - 421. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-H. Seo, A. Suenaga, M. Hatakeyama, M. Taiji, and A. Imamoto Structural and Functional Basis of a Role for CRKL in a Fibroblast Growth Factor 8-Induced Feed-Forward Loop Mol. Cell. Biol., June 1, 2009; 29(11): 3076 - 3087. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Rochais, K. Mesbah, and R. G. Kelly Signaling Pathways Controlling Second Heart Field Development Circ. Res., April 24, 2009; 104(8): 933 - 942. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. R. Chien, I. J. Domian, and K. K. Parker Cardiogenesis and the Complex Biology of Regenerative Cardiovascular Medicine Science, December 5, 2008; 322(5907): 1494 - 1497. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Zhang, Y. Lin, Y. Zhang, Y. Lan, C. Lin, A. M. Moon, R. J. Schwartz, J. F. Martin, and F. Wang Frs2{alpha}-deficiency in cardiac progenitors disrupts a subset of FGF signals required for outflow tract morphogenesis Development, November 1, 2008; 135(21): 3611 - 3622. [Abstract] [Full Text] [PDF]
|
|
