Transduction of the signal initiated by the neuropeptide, testis ecdysiotropin, in testes of the gypsy moth, Lymantria dispar

Abstract

Testes of Lymantria dispar synthesize immunologically detectable ecdysteroid in vitro. Early last instar larval testes can be induced to produce ecdysteroid de novo by means of the brain peptide, testis ecdysiotropin (TE), although testes excised in mid pupal stage synthesize ecdysteroid without TE stimulus in vitro; they can be boosted to higher levels of synthesis with TE. By use of agents H-7 and H-8, inhibitors of phosphokinases C (PKC) and cAMP-dependent protein kinase (PKA), respectively, we have confirmed previous data indicating that diacyl glycerol and its effector, PKC, are second messengers for the TE message. In larval testes, but not pupal testes, cAMP and PKA also regulate ecdysteroid synthesis. Data obtained from incubation of testes with analogs of GTP (GTPγS) and GDP (GDPβS) and the ribosylating agents, pertussis and cholera toxins, indicate that TE is transduced via inhibiting G protein (G i) in larval testes, although both G i and stimulating G protein (G s) influence ecdysteroid synthesis in pupal testes. Synthesis must be further modulated by feedback loops operating with G s and G i controlled factors in testes exposed to TE. Ecdysteroid synthesis appears to be constitutive in pupal testes in the absence of exogenous TE.