ZFIN ID: ZDB-PUB-081218-20
The Sphingolipid Transporter Spns2 Functions in Migration of Zebrafish Myocardial Precursors
Kawahara, A., Nishi, T., Hisano, Y., Fukui, H., Yamaguchi, A., and Mochizuki, N.
Date: 2009
Source: Science (New York, N.Y.)   323(5913): 524-527 (Journal)
Registered Authors: Kawahara, Atsuo
Keywords: none
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Blastomeres/metabolism
  • CHO Cells
  • Carrier Proteins/chemistry
  • Carrier Proteins/genetics
  • Carrier Proteins/metabolism*
  • Cell Movement
  • Cricetinae
  • Cricetulus
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/metabolism*
  • Embryonic Development
  • Heart/embryology*
  • Heart Defects, Congenital/embryology
  • Humans
  • Lysophospholipids/metabolism*
  • Membrane Proteins/chemistry
  • Membrane Proteins/genetics
  • Membrane Proteins/metabolism*
  • Mesoderm/metabolism
  • Mice
  • Molecular Sequence Data
  • Mutation
  • Oligonucleotides, Antisense
  • Organogenesis
  • Signal Transduction
  • Somites/embryology
  • Somites/metabolism
  • Sphingosine/analogs & derivatives*
  • Sphingosine/metabolism
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish Proteins/chemistry
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed: 19074308 Full text @ Science
FIGURES
ABSTRACT
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, which displays cardia bifida (two hearts) resembling 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 extra-embryonic tissue yolk syncytial layer (YSL) and 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.
ADDITIONAL INFORMATION