| First Author | Brûlé E | Year | 2021 |
| Journal | Sci Adv | Volume | 7 |
| Issue | 51 | Pages | eabl4391 |
| PubMed ID | 34910520 | Mgi Jnum | J:316383 |
| Mgi Id | MGI:6835794 | Doi | 10.1126/sciadv.abl4391 |
| Citation | Brule E, et al. (2021) TGFBR3L is an inhibin B co-receptor that regulates female fertility. Sci Adv 7(51):eabl4391 |
| abstractText | Follicle-stimulating hormone (FSH), a key regulator of ovarian function, is often used in infertility treatment. Gonadal inhibins suppress FSH synthesis by pituitary gonadotrope cells. The TGFβ type III receptor, betaglycan, is required for inhibin A suppression of FSH. The inhibin B co-receptor was previously unknown. Here, we report that the gonadotrope-restricted transmembrane protein, TGFBR3L, is the elusive inhibin B co-receptor. TGFBR3L binds inhibin B but not other TGFbeta family ligands. TGFBR3L knockdown or overexpression abrogates or confers inhibin B activity in cells. Female Tgfbr3l knockout mice exhibit increased FSH levels, ovarian follicle development, and litter sizes. In contrast, female mice lacking both TGFBR3L and betaglycan are infertile. TGFBR3Lâs function and cell-specific expression make it an attractive new target for the regulation of FSH and fertility. |
