TGFBR3L is an inhibin B co-receptor that regulates female fertility

Emilie Brule, Ying Wang, Yining Li, Yeu Farn Lin, Xiang Zhou, Luisina Ongaro, Carlos A.I. Alonso, Evan R.S. Buddle, Alan L. Schneyer, Chang Hyeock Byeon, Cynthia S. Hinck, Natalia Mendelev, John P. Russell, Mitra Cowan, Ulrich Boehm, Frederique Ruf-Zamojski, Michel Zamojski, Cynthia L. Andoniadou, Stuart C. Sealfon, Craig A. HarrisonKelly L. Walton, Andrew P. Hinck, Daniel J. Bernard

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

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 TGFβ 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. TGFBR3L's function and cell-specific expression make it an attractive new target for the regulation of FSH and fertility.

Original languageEnglish
Article numbereabl4391
JournalScience advances
Volume7
Issue number51
DOIs
StatePublished - Dec 2021

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