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Background  Lysophospholipids such as lysophosphatidic acid (LPA) and sphingosine-1-phosphate (S1P) are important signaling molecules that can regulate a wide range of cellular responses. We discovered that  Sphingosine kinase 1  ( Sphk1 ), a key enzyme that converts sphingosine to S1P, is expressed in neurons and progenitor cells in nascent trigeminal and dorsal root ganglia during mouse embryogenesis.    Methods and Findings    Sphk1  null mouse embryos do not display overt deficits owing to compensation by  Sphk2 . Thus, we analyzed embryos that are deficient in both  Sphk1  and  Sphk2  (which essentially eliminates S1P function) in order to investigate the role(s) of  Sphk1  during sensory ganglia formation. While animals lacking 1–3 alleles of  Sphk1  and  Sphk2  had no obvious phenotype, embryos without both genes displayed clear developmental defects. The complete absence of  Sphk1  and  Sphk2  resulted in trigeminal and dorsal root ganglia with fewer neurons and progenitor cells. The profound loss in cell number could be attributed to a decrease in cell proliferation as well as an increase in apoptosis. Furthermore,  Sphk1 / 2  double mutants displayed an overall reduction in other sphingolipids as well as an imbalance of S1P/sphingosine and S1P/ceramide ratio, thereby favoring cell death and reducing cell growth.    Conclusions  Together, these results provide strong in vivo evidence that sphingosine kinase/S1P signaling plays an important role in regulating early events during development of sensory ganglia.

Loss of Sphingosine Kinase 1/S1P Signaling Impairs Cell Growth and Survival of Neurons and Progenitor Cells in the Developing Sensory Ganglia