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, Hidefumi Yoshioka

Research output: Contribution to journalArticlepeer-review

79 Citations (Scopus)


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 Ad4BPISF-1 and estrogen receptor α 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, Ad4BPISF-1, estrogen receptor α and cyclin D1.

Original languageEnglish
Pages (from-to)677-685
Number of pages9
Issue number4
Publication statusPublished - Feb 2008

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Developmental Biology


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