title: Mesonephric FGF signaling is associated with the development of sexually indifferent gonadal primordium in chick embryos.
abstract: The gonad as well as the reproductive tracts, kidney, and adrenal cortex are derived from the intermediate mesoderm. In addition, the intermediate mesoderm forms the mesonephros. Although the mesonephros is the source of certain testicular cell types, its contribution to gonad formation through expression of growth factors is largely unknown. Here, we examined the expression profiles of FGF9 in the developing mesonephros of chick embryos at sexually indifferent stages, and found that the expression domain is adjacent to the gonadal primordium. Moreover, FGFR3 (FGF receptor 3) showed a strong expression in the gonadal primordium. Next, we examined the functions of FGF signal during gonadal development with misexpressed FGF9. Interestingly, misexpression of FGF9 led to gonadal expansion through stimulation of cell proliferation. In contrast, treatment with a chemical inhibitor for FGFR decreased cell proliferation and resulted in reduction of the gonadal size. Simultaneously, the treatment resulted in reduction of gonadal marker gene expression. Our study demonstrated that FGF expressed in the developing mesonephros is involved in the development of the gonad at the sexually indifferent stages through stimulation of gonadal cell proliferation and gonadal marker gene expression.
authors.affiliation: Department of Natural Sciences, Hyogo University of Teacher Education, 942-1, Yashiro-cho, Kato Gun, Hyogo 673-1494, Japan.
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Yoshioka
authors.forename: Yoshiyasu
authors.initials: Y
authors.lastname: Ishimaru
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Sugiyama
authors.forename: Naoki
authors.initials: N
authors.lastname: Tsunekawa
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Noce
authors.forename: Megumi
authors.initials: M
authors.lastname: Kasahara
authors.forename: Ken-ichirou
authors.initials: K
authors.lastname: Morohashi
mesh_terms: D000818:Animals; D015415:Biomarkers; D049109:Cell Proliferation; D002642:Chick Embryo; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D051525:Fibroblast Growth Factor 9; D005346:Fibroblast Growth Factors / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D006066:Gonads / Q000196:embryology* / Q000502:physiology; D018398:Homeodomain Proteins; D017403:In Situ Hybridization; D008650:Mesonephros / Q000196:embryology* / Q000378:metabolism*; D051379:Mice; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D011758:Pyrroles / Q000378:metabolism; D051498:Receptor, Fibroblast Growth Factor, Type 3; D018160:Receptors, Cytoplasmic and Nuclear; D017468:Receptors, Fibroblast Growth Factor / Q000235:genetics / Q000378:metabolism; D012733:Sex Differentiation; D015398:Signal Transduction / Q000502:physiology*; D054339:Steroidogenic Factor 1; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D015415:Biomarkers; C110547:DMRT1 protein; D004268:DNA-Binding Proteins; C496460:Fgf9 protein, mouse; D051525:Fibroblast Growth Factor 9; D018398:Homeodomain Proteins; D011758:Pyrroles; D018160:Receptors, Cytoplasmic and Nuclear; D017468:Receptors, Fibroblast Growth Factor; C105686:SU 5402; D054339:Steroidogenic Factor 1; D014157:Transcription Factors; D005346:Fibroblast Growth Factors; C496366:Fgfr3 protein, mouse; D011505:Protein-Tyrosine Kinases; D051498:Receptor, Fibroblast Growth Factor, Type 3