Meeting Abstract

P3.115  Tuesday, Jan. 6  A serotonin-mediated signaling mechanism initiates cell movements during sea urchin gastrulation SCULLY, T.A.*; CARROLL, K.N.; BROWN, K.M.; The George Washinton University tscully@gwu.edu

Previous studies in our lab have identified several components of a serotonergic system in blastula and gastrula sea urchin embryos. These studies suggest that serotonin regulates gastrulation. In the present study we examined the role of the serotonin synthetic enzyme, tryptophan hydroxylase (TPH), in sea urchin embryogenesis. Embryos were treated with various concentrations(0.5 – 20 M)of p-chlorophenylalanine methyl ester(methyl-CPA), an inhibitor of TPH, beginning at fertilization or at the hatched blastula stage. Cleavage was not affected, and embryo development stopped prior to gastrulation at the mesenchyme blastula stage with higher concentrations of the drug. Lower concentrations blocked development at the early gastrula stage. The lowest levels of methyl-CPA to exert effects delayed gastrulation beyond the early gastrula stage. Serotonin (100 M) or dibutyryl cyclic AMP(1 M), added along with the inhibitor (20 M) at hatching, rescued embryos from the inhibitory effects of methyl-CPA on early gastrulation. Methyl-CPA also inhibited TPH activity in enzyme assays of embryo homogenates. The nonmethylated inhibitor (CPA)did not inhibit gastrulation. This study suggests methyl-CPA specifically blocks serotonin synthesis and inhibits gastrulation, and serotonin regulates the primary gastrulation phase by signaling mechanism(s)that involve cyclic AMP.