title: GnRH signaling pathways regulate differentially the tilapia gonadotropin subunit genes.
abstract: Exposure of tilapia pituitary cells in culture to salmon gonadotropin-releasing hormone (sGnRH; 0.01-100 nM) elevated the phosphorylated extracellular signal-regulated kinase (pERK) levels. sGnRH also elevated the alpha, FSHbeta and LHbeta subunit mRNA levels. The phorbol ester, 1-O-tetradecanoyl phorbol-13-acetate (TPA; 12.5 nM) increased pERK levels, whereas protein kinase C (PKC) depletion or inhibition by GF109203X (GF; 0.01-10 microM) suppressed GnRH-activated ERKs. GF too abated the GnRH-induced alpha and LHbeta mRNA levels, but had no effect on those of FSHbeta. Forskolin (0.001-100 microM) activated ERK, while inhibition of protein kinase A (PKA) by H89 (0.01-10 microM) suppressed pERK levels and all GnRH-stimulated gonadotropin subunit transcripts. Exposure of cells to the mitogen-activated protein kinase kinase (MAPK kinase; MEK) inhibitor (PD98059; PD 10, 25 and 50 microM) completely blocked GnRH-induced increase in ERKs activation. Furthermore, PD suppressed the alpha and LHbeta mRNA responses to GnRH, but had no effect on FSHbeta mRNA levels. It is suggested that in tilapia the differential regulation of gonadotropin subunit gene expression by GnRH results from a divergent recruitment of signal transduction pathways, activated upon GnRH binding; PKC-ERK cascade is involved in elevating alpha and LHbeta mRNAs, whereas induction of FSHbeta transcript is ERK-independent and is under direct cAMP-PKA regulation or through other MAPK cascades.
authors.affiliation: Department of Zoology, Tel-Aviv University, 69978, Tel Aviv, Israel.
authors.forename: G
authors.initials: G
authors.lastname: Gur
authors.forename: D
authors.initials: D
authors.lastname: Bonfil
authors.forename: H
authors.initials: H
authors.lastname: Safarian
authors.forename: Z
authors.initials: Z
authors.lastname: Naor
authors.forename: Z
authors.initials: Z
authors.lastname: Yaron
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology*; D006065:Gonadotropins, Pituitary / Q000235:genetics* / Q000378:metabolism; D007211:Indoles / Q000494:pharmacology; D008297:Male; D008301:Maleimides / Q000494:pharmacology; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D010902:Pituitary Gland / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism; D021122:Protein Subunits; D012474:Salmon / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects* / Q000502:physiology; D017210:Tilapia / Q000502:physiology*
chemical_list: D004791:Enzyme Inhibitors; D006065:Gonadotropins, Pituitary; D007211:Indoles; D008301:Maleimides; D021122:Protein Subunits; D007987:Gonadotropin-Releasing Hormone; D017868:Cyclic AMP-Dependent Protein Kinases; D011493:Protein Kinase C; D020928:Mitogen-Activated Protein Kinases; C070515:bisindolylmaleimide I