Useful cooperation of spns2 and fibronectin in cardiac and reduce jaw advancement [Investigation Article]
oneLaboratory for Cardiovascular Molecular Dynamics, Riken Quantitative Biology Heart, Furuedai six-2-3, Suita, Osaka 565-0874, Japan
2Okazaki Institute for Integrative Bioscience, National Institute of Normal Sciences, Okazaki, Aichi 444-8787, Japan
threeDepartment of Basic Biology, The Graduate College for Advanced Studies (SOKENDAI), Okazaki, Aichi 444-8787, Japan
- ↵*Author for correspondence ( )
The lipid mediator sphingosine-1-phosphate (S1P) is a regulator of cardiac development in zebrafish, as disruption of its
receptor s1pr2 or transporter spns2 leads to migration defects in cardiac progenitors. To examine the genetic conversation of S1P signaling and the mobile adhesion
molecule fibronectin, we have proven a fnspns2 double mutant. Cardiac migration flaws in fnspns2 mutants were far more serious than people in fn or spns2 mutants. We further identified that the reduce jaw morphology was disorganized in the fnspns2 mutant, although it experienced a marginally shortened anterior–posterior distance in the ventral pharyngeal arch in fn and spns2 mutants relative to wild variety. Knockdown of fn in the s1pr2 mutant, but not in the s1pr1 mutant, resulted in extreme defects in cardiac migration and ventral pharyngeal arch arrangement. Additional, in the history
of the fn mutant, knockdown of endothelin receptor A (ednra), which was downregulated in the spns2 mutant, triggered pharyngeal flaws resembling these in the fnspns2 mutant. These results strongly advise that Spns2-S1PR2 signaling and fibronectin cooperatively control both cardiac and
reduced jaw advancement in zebrafish.
- Acquired April seven, 2013.
- Recognized May possibly 29, 2013.
- © 2013. Printed by The Firm of Biologists Ltd
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