Estrogen receptor 2b is the major determinant of sex-typical mating behavior and sexual preference in medaka
Estrogen receptor 2b is the major determinant of sex-typical mating behavior and sexual preference in medaka
复制标题
雌激素受体 2b 是青鳉性别典型交配行为和性偏好的主要决定因素
DOI：
10.1016/j.cub.2021.01.089
复制
发表时间：
2021
期刊：
影响因子：
9.2
通讯作者：
Okubo Kataaki
中科院分区：
文献类型：
--
作者：
Nishiike Yuji;Miyazoe Daichi;Togawa Rie;Yokoyama Keiko;Nakasone Kiyoshi;Miyata Masayoshi;Kikuchi Yukiko;Kamei Yasuhiro;Todo Takeshi;Ishikawa-Fujiwara Tomoko;Ohno Kaoru;Usami Takeshi;Nagahama Yoshitaka;Okubo Kataaki
雄性和雌性动物通常表现出先天的性别特异性交配行为，在脊椎动物中，这高度依赖于性类固醇信号。虽然雌二醇-17 β（E2）信号通过雌激素受体2（ESR 2）在啮齿动物中起到使雄性交配行为去雌性化的作用，但现有证据表明，在硬骨鱼类中，雄性或雌性交配行为不需要E2信号。在这里，我们报告说，女性青鳉缺乏ESR 2b，ESR 2的硬骨鱼直系同源，不接受男性，而是法院的女性，尽管保留正常的卵巢功能与未改变的性类固醇环境。因此，与啮齿动物和硬骨鱼的流行观点相反，大脑中的E2/Esr 2b信号在青鳉雌性交配行为和性偏好的女性化和去男性化中起着决定性作用。进一步的行为测试表明，成年期E2/Esr 2b信号和雄激素受体介导的雄激素信号之间的相互拮抗作用诱导并积极维持性典型的交配行为和偏好。我们的研究结果还表明，女性偏见的性二型性inesr 2b在端脑和视前核的表达，涉及交配行为，可以逆转男性和女性之间的性类固醇环境在成年期，可能通过机制，涉及直接E2诱导的转录激活。此外，Npba，一种调节女性性感受性的神经肽，被发现在这些脑核团中作用于E2/Esr 2b信号的下游。总的来说，E2/Esr 2b信号的这些功能和调节机制可能是硬骨鱼类（至少在青鳉中）诱导、维持和逆转性典型交配行为和性偏好的神经机制的基础。
Male and female animals typically display innate sex-specific mating behaviors, which, in vertebrates, are highly dependent on sex steroid signaling. While estradiol-17β (E2) signaling through estrogen receptor 2 (ESR2) serves to defeminize male mating behavior in rodents, the available evidence suggests that E2 signaling is not required in teleosts for either male or female mating behavior. Here, we report that female medaka deficient for Esr2b, a teleost ortholog of ESR2, are not receptive to males but rather court females, despite retaining normal ovarian function with an unaltered sex steroid milieu. Thus, contrary to both prevailing views in rodents and teleosts, E2/Esr2b signaling in the brain plays a decisive role in feminization and demasculinization of female mating behavior and sexual preference in medaka. Further behavioral testing showed that mutual antagonism between E2/Esr2b signaling and androgen receptor-mediated androgen signaling in adulthood induces and actively maintains sex-typical mating behaviors and preference. Our results also revealed that the female-biased sexual dimorphism inesr2bexpression in the telencephalic and preoptic nuclei implicated in mating behavior can be reversed between males and females by altering the sex steroid milieu in adulthood, likely via mechanisms involving direct E2-induced transcriptional activation. In addition, Npba, a neuropeptide mediating female sexual receptivity, was found to act downstream of E2/Esr2b signaling in these brain nuclei. Collectively, these functional and regulatory mechanisms of E2/Esr2b signaling presumably underpin the neural mechanism for induction, maintenance, and reversal of sex-typical mating behaviors and sexual preference in teleosts, at least in medaka.