Comprehensive analysis of sphingosine‐1‐phosphate receptor mutants during zebrafish embryogenesis. (11th June 2015)

• Record Type: Journal Article
• Authors: Hisano, Yu; Inoue, Asuka; Taimatsu, Kiyohito; Ota, Satoshi; Ohga, Rie; Kotani, Hirohito; Muraki, Michiko; Aoki, Junken; Kawahara, Atsuo
• Is Part Of: Genes to cells. Volume 20:Number 8(2015:Aug.)
• Page Start: 647
• Page End: 658
• Publication Date: 2015-06-11
• Subjects: Cytogenetics -- Periodicals; Cells -- Mechanical properties -- Periodicals; Molecular genetics -- Periodicals; Genes -- Periodicals; Molecular biology -- Periodicals; Cytology -- Periodicals; Biomechanics -- Periodicals; 571.6
• DOI: 10.1111/gtc.12259
• Languages: English
• ISSNs: 1356-9597

Abstract

<abstract abstract-type="main" id="gtc12259-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>The lipid mediator sphingosine‐1‐phosphate (S1P) regulates various physiological and pathological phenomena such as angiogenesis and oncogenesis. Secreted S1P associates with the G‐protein‐coupled S1P receptors (S1PRs), leading to the activation of downstream signaling molecules. In mammals, five <italic>S1prs</italic> have been identified and the genetic disruption of a single <italic>S1pr1</italic> gene causes vascular defects. In zebrafish, seven <italic>s1prs</italic> have been isolated. We found that individual <italic>s1prs</italic> showed unique expression patterns with some overlapping expression domains during early embryogenesis. We generated all <italic>s1pr</italic> single‐mutant zebrafish by introducing premature stop codons in their coding regions using transcription activator‐like effector nucleases and analyzed their phenotypes during early embryogenesis. Zygotic <italic>s1pr1</italic>, <italic> s1pr3a</italic>, <italic> s1pr3b</italic>, <italic> s1pr4</italic>, <italic> s1pr5a</italic> and <italic>s1pr5b</italic> mutants showed no developmental defects and grew into adults, whereas zygotic <italic>s1pr2</italic> mutant showed embryonic lethality with a cardiac defect, showing quite distinct embryonic phenotypes for individual <italic>S1pr</italic> mutants between zebrafish and mouse. We further generated maternal‐zygotic <italic>s1pr1</italic>, <italic> s1pr3a</italic>, <italic> s1pr3b</italic>, <italic> s1pr4</italic>, <italic> s1pr5a</italic> and <italic>s1pr5b</italic> mutants and found that these maternal‐zygotic mutants also showed no obvious developmental defects, presumably suggesting the redundant functions of the S1P receptor‐mediated signaling in zebrafish.</p> </abstract>