Mechanism of asymmetric ovarian development in chick embryos
Author:
Ishimaru Yoshiyasu12, Komatsu Tomoko2, Kasahara Megumi1, Katoh-Fukui Yuko2, Ogawa Hidesato2, Toyama Yoshiro3, Maekawa Mamiko3, Toshimori Kiyotaka3, Chandraratna Roshantha A. S.4, Morohashi Ken-ichirou2, Yoshioka Hidefumi1
Affiliation:
1. Department of Natural Sciences, Hyogo University of Teacher Education, 942-1,Shimokume, Kato, Hyogo 673-1494, Japan. 2. Division for Sex Differentiation, National Institute for Basic Biology,National Institutes of Natural Sciences, Myodaijicho, Okazaki, Aichi 444-8787,Japan. 3. Department of Anatomy and Developmental Biology, Graduate School of Medicine,Chiba University, Chiba 260-8670, Japan. 4. Retinoid Research, Departments of Chemistry and Biology, Allergan, Irvine, CA 92623, USA.
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 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,Ad4BP/SF-1, estrogen receptor α and cyclin D1.
Publisher
The Company of Biologists
Subject
Developmental Biology,Molecular Biology
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