Mechanism of asymmetric ovarian development in chick embryos
Mechanism of asymmetric ovarian development in chick embryos
复制标题
DOI：
10.1242/dev.012856
复制
发表时间：
2008-02-15
期刊：
影响因子：
4.6
通讯作者：
Yoshioka, Hidefumi
中科院分区：
文献类型：
--
作者：
Ishimaru, Yoshiyasu;Komatsu, Tomoko;Yoshioka, Hidefumi
在大多数动物中，性腺是对称发育的，但大多数鸟类只发育一个左卵巢。雌激素在小鸡卵巢不对称发育中可能起作用，但这一过程的机制尚不清楚。在这里，我们确定了这种卵巢不对称的分子机制。PITX2在左侧推定性腺中的不对称表达导致视黄酸（RA）合成酶RALDH 2在右侧推定性腺中的不对称表达。随后，RA抑制核受体Ad4BP/SF-1和雌激素受体α在右侧卵巢原基中的表达。在左侧卵巢原基中表达的Ad4BP/SF-1不对称地上调细胞周期蛋白D1以刺激细胞增殖。这些数据表明，PITX2的早期不对称表达通过上调或下调RALDH 2、Ad4BP/SF-1、雌激素受体α和细胞周期蛋白D1导致卵巢发育不对称。
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.