Steroidogenic factor 1 regulates transcription of the inhibin B co-receptor in pituitary gonadotrope cells

Yeu Farn Lin, Gauthier Schang, Evan R S Buddle, Hailey Schultz, Thea L Willis, Frederique Ruf-Zamojski, Michel Zamojski, Natalia Mendelev, Ulrich Boehm, Stuart C Sealfon, Cynthia L Andoniadou, Daniel J Bernard

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The inhibins control reproduction by suppressing follicle-stimulating hormone synthesis in pituitary gonadotrope cells. The newly discovered inhibin B co-receptor, TGFBR3L, is selectively and highly expressed in gonadotropes in both mice and humans. Here, we describe our initial characterization of mechanisms controlling cell-specific Tgfbr3l/TGFBR3L transcription. We identified two steroidogenic factor 1 (SF-1 or NR5A1) cis-elements in the proximal Tgfbr3l promoter in mice. SF-1 induction of murine Tgfbr3l promoter-reporter activity was inhibited by mutations in one or both sites in heterologous cells. In homologous cells, mutation of these cis-elements or depletion of endogenous SF-1 similarly decreased reporter activity. We observed nearly identical results when using a human TGFBR3L promoter-reporter. The Tgfbr3l gene was tightly compacted and Tgfbr3l mRNA expression was essentially absent in gonadotropes of SF-1 (Nr5a1) conditional knockout mice. During murine embryonic development, Tgfbr3l precedes Nr5a1 expression, though the two transcripts are fully co-localized by embryonic day 18.5 and thereafter. Collectively, these data indicate that SF-1 directly regulates Tgfbr3l/TGFBR3L transcription and is required for post-natal expression of the gene in gonadotropes.

Original languageEnglish
Article numberbqac131
Issue number11
Early online date12 Aug 2022
Publication statusE-pub ahead of print - 12 Aug 2022


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