4.8 Article

Estrogen receptor 2b is the major determinant of sex-typical mating behavior and sexual preference in medaka

期刊

CURRENT BIOLOGY
卷 31, 期 8, 页码 1699-+

出版社

CELL PRESS
DOI: 10.1016/j.cub.2021.01.089

关键词

-

资金

  1. Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Japan
  2. Japan Society for the Promotion of Science (JSPS) (MEXT/JSPS) [16H04979, 17H06429, 19H03044]
  3. Grants-in-Aid for Scientific Research [19H03044, 16H04979, 17H06429] Funding Source: KAKEN

向作者/读者索取更多资源

The study reveals that in medaka, E2/Esr2b signaling in the brain plays a decisive role in feminization and demasculinization of female mating behavior and sexual preference, which contrasts with prevailing views in rodents and other teleosts. The mutual antagonism between E2/Esr2b signaling and androgen receptor-mediated androgen signaling induces and actively maintains sex-typical mating behaviors and preference in adulthood. Female-biased sexual dimorphism in esr2b expression in specific brain nuclei associated with mating behavior can be reversed between males and females by altering the sex steroid environment in adulthood.
Male and female animals typically display innate sex-specific mating behaviors, which, in vertebrates, are highly dependent on sex steroid signaling. While estradiol-17b (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 in esr2b expression 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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.8
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据