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First published online September 28, 2006
doi: 10.1242/10.1242/dev.02581
1 Department of Biochemistry and Biophysics and Programs in Developmental
Biology, Genetics and Human Genetics, Cardiovascular Research Institute,
University of California, San Francisco, San Francisco, CA 94143-2711,
USA.
2 Division of Biological Science, Graduate School of Science, Nagoya University,
Furo-cho, Chikusa-ku, Nagoya 464-8602, Japan.
3 Department of Biological Sciences, Graduate School of Science, University of
Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan.
* Authors for correspondence (e-mail: htakeda{at}biol.s.u-tokyo.ac.jp; didier_stainier{at}biochem.ucsf.edu)
Accepted 10 August 2006
The roles of extra-embryonic tissues in early vertebrate body patterning have been extensively studied, yet we know little about their function during later developmental events. Here, we analyze the function of the zebrafish extra-embryonic yolk syncytial layer (YSL) specific transcription factor, Mtx1, and find that it plays an essential role in myocardial migration. Downregulating the function of Mtx1 in the YSL leads to cardia bifida, a phenotype in which the myocardial cells fail to migrate to the midline. Mtx1 in the extra-embryonic YSL appears to regulate the embryonic expression of fibronectin, a gene previously implicated in myocardial migration. We further show dosage-sensitive genetic interactions between mtx1 and fibronectin. Based on these data, we propose that the extra-embryonic YSL regulates myocardial migration, at least in part by influencing fibronectin expression and subsequent assembly of the extracellular matrix in embryonic tissues.
Key words: Myocardial migration, mtx1 (mxtx1), Yolk syncytial layer (YSL), fibronectin, natter, Zebrafish
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