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Development ePress online publication date 16 Jan 2008
doi: 10.1242/dev.012856

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Research article

Mechanism of asymmetric ovarian development in chick embryos


Yoshiyasu Ishimaru, Tomoko Komatsu, Megumi Kasahara, Yuko Katoh-Fukui, Hidesato Ogawa, Yoshiro Toyama, Mamiko Maekawa, Kiyotaka Toshimori, Roshantha A.S. Chandraratna, Ken-ichirou Morohashi*, and Hidefumi Yoshioka
* Author for correspondence (e-mail: moro{at}nibb.ac.jp)

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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