Journal
SCIENCE
Volume 323, Issue 5913, Pages 524-527Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1167449
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Funding
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- National BioResource Project of Japan
- Japan Society for the Promotion of Science
- Program for the Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation
- Ministry of Health, Labor and Welfare of Japan
- Takeda Science Foundation
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Sphingosine-1-phosphate ( S1P) is a secreted lipid mediator that functions in vascular development; however, it remains unclear how S1P secretion is regulated during embryogenesis. We identified a zebrafish mutant, ko157, that displays cardia bifida ( two hearts) resembling that in the S1P receptor- 2 mutant. A migration defect of myocardial precursors in the ko157 mutant is due to a mutation in a multipass transmembrane protein, Spns2, and can be rescued by S1P injection. We show that the export of S1P from cells requires Spns2. spns2 is expressed in the extraembryonic tissue yolk syncytial layer ( YSL), and the introduction of spns2 mRNA in the YSL restored the cardiac defect in the ko157 mutant. Thus, Spns2 in the YSL functions as a S1P transporter in S1P secretion, thereby regulating myocardial precursor migration.
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