Meeting Abstract
Knowledge of the mechanisms regulating sperm motility would enable the development of more reliable methods to improve sperm quality and spawning of marine fish in captivity. Acute treatment of southern flounder and Atlantic croaker sperm in vitro with a teleost progestin hormone (20β-S) causes rapid induction of sperm hypermotility and increased fertility through activation of progestin membrane receptor alpha (mPRα,Paqr7) coupled to a stimulatory G protein. The involvement of several intracellular signaling pathways in the sperm hypermotility response to 20β-S was investigated by incubation with inhibitors (I) or activators (A) of Egfr (I:AG1478, A:EGF), Mapk/Erk1/2 (I: U0126), Pi3k/Akt (Pi3k I:Wortmannin, LY294002, Akt I: ML9), Acy/cAMP (I: dd-Ado, A: forskolin), Pde (I: Cilostamide), or calcium (L-type channel I:verapamil) signaling pathways for 30 min. prior to treatment with 20β-S or Org 02-0 (specific mPR agonist) for 1 min. and motility activation with a hyperosmotic medium. The induction of sperm hypermotility by 20β-S and Org 02-0 was blocked by prior treatments with inhibitors of Egfr, Mapk, Pi3k/Akt, Pde, and Acy. On the other hand treatment with activators of Egfr (EGF) and Acy (forskolin) mimicked the effects of the progestins and induced sperm hypermotility. These results indicate that progestins induce sperm hypermotility through Egfr/Mapk/Erk1/2, Pi3k/Akt/Pde, and Acy/cAMP pathways. The progestins caused rapid calcium influx into sperm, an effect blocked by verapamil which also blocked progestin-induced sperm hypermotility. The results suggest progestins activate multiple signaling pathways through mPRα in flounder sperm to induce calcium influx and hypermotility and enhance fertility.
