Poirier Christophe, Qin Yangjun, Adams Carolyn P, Anaya Yanett, Singer Jonathan B, Hill Annie E, Lander Eric S, Nadeau Joseph H, Bishop Colin E
Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas 77030, USA.
Genetics. 2004 Nov;168(3):1557-62. doi: 10.1534/genetics.104.032177.
The transgenic insertional mouse mutation Odd Sex (Ods) represents a model for the long-range regulation of Sox9. The mutation causes complete female-to-male sex reversal by inducing a male-specific expression pattern of Sox9 in XX Ods/+ embryonic gonads. We previously described an A/J strain-specific suppressor of Ods termed Odsm1(A). Here we show that phenotypic sex depends on a complex interaction between the suppressor and the transgene. Suppression can be achieved only if the transgene is transmitted paternally. In addition, the suppressor itself exhibits a maternal effect, suggesting that it may act on chromatin in the early embryo.
转基因插入小鼠突变体“奇特性别”(Odd Sex,Ods)代表了一种Sox9基因远程调控的模型。该突变通过在XX Ods/+胚胎性腺中诱导Sox9的雄性特异性表达模式,导致完全的雌性向雄性性反转。我们之前描述了一种名为Odsm1(A)的Ods的A/J品系特异性抑制因子。在此我们表明,表型性别取决于抑制因子与转基因之间的复杂相互作用。只有当转基因通过父系传递时才能实现抑制。此外,抑制因子本身表现出母系效应,这表明它可能在早期胚胎中作用于染色质。