title: Mechanism of asymmetric ovarian development in chick embryos.
abstract: In most animals, the gonads develop symmetrically, but most birds develop only a left ovary. A possible role for estrogen in this asymmetric ovarian development has been proposed in the chick, but the mechanism underlying this process is largely unknown. Here, we identify the molecular mechanism responsible for this ovarian asymmetry. Asymmetric PITX2 expression in the left presumptive gonad leads to the asymmetric expression of the retinoic-acid (RA)-synthesizing enzyme, RALDH2, in the right presumptive gonad. Subsequently, RA suppresses expression of the nuclear receptors Ad4BP/SF-1 and estrogen receptor alpha in the right ovarian primordium. Ad4BP/SF-1 expressed in the left ovarian primordium asymmetrically upregulates cyclin D1 to stimulate cell proliferation. These data suggest that early asymmetric expression of PITX2 leads to asymmetric ovarian development through up- or downregulation of RALDH2, Ad4BP/SF-1, estrogen receptor alpha and cyclin D1.
authors.affiliation: Department of Natural Sciences, Hyogo University of Teacher Education, 942-1, Shimokume, Kato, Hyogo 673-1494, Japan.
authors.forename: Yoshiyasu
authors.initials: Y
authors.lastname: Ishimaru
authors.forename: Tomoko
authors.initials: T
authors.lastname: Komatsu
authors.forename: Megumi
authors.initials: M
authors.lastname: Kasahara
authors.forename: Yuko
authors.initials: Y
authors.lastname: Katoh-Fukui
authors.forename: Hidesato
authors.initials: H
authors.lastname: Ogawa
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Toyama
authors.forename: Mamiko
authors.initials: M
authors.lastname: Maekawa
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Toshimori
authors.forename: Roshantha A S
authors.initials: RA
authors.lastname: Chandraratna
authors.forename: Ken-ichirou
authors.initials: K
authors.lastname: Morohashi
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Yoshioka
mesh_terms: D000818:Animals; D019521:Body Patterning / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002642:Chick Embryo; D019938:Cyclin D1 / Q000235:genetics / Q000378:metabolism; D003577:Cytochrome P-450 Enzyme System / Q000235:genetics / Q000378:metabolism; D047628:Estrogen Receptor alpha / Q000235:genetics / Q000378:metabolism; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism; D008954:Models, Biological; D010053:Ovary / Q000166:cytology / Q000187:drug effects / Q000196:embryology* / Q000201:enzymology; D000072516:Retinoic Acid 4-Hydroxylase; D019849:Sex Determination Processes; D015398:Signal Transduction / Q000187:drug effects; D054339:Steroidogenic Factor 1 / Q000235:genetics / Q000378:metabolism; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D014212:Tretinoin / Q000494:pharmacology; D000097577:Homeobox Protein PITX2
chemical_list: D019938:Cyclin D1; D003577:Cytochrome P-450 Enzyme System; D047628:Estrogen Receptor alpha; D018398:Homeodomain Proteins; D000072516:Retinoic Acid 4-Hydroxylase; D054339:Steroidogenic Factor 1; D014157:Transcription Factors; D014212:Tretinoin; D000097577:Homeobox Protein PITX2