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Mechanism of asymmetric ovarian development in chick embryos
Authors:Ishimaru Yoshiyasu  Komatsu Tomoko  Kasahara Megumi  Katoh-Fukui Yuko  Ogawa Hidesato  Toyama Yoshiro  Maekawa Mamiko  Toshimori Kiyotaka  Chandraratna Roshantha A S  Morohashi Ken-ichirou  Yoshioka Hidefumi
Institution:Department of Natural Sciences, Hyogo University of Teacher Education, 942-1, Shimokume, Kato, Hyogo 673-1494, Japan.
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.
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