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Successful mammalian reproduction depends on proper synthesis of the pituitary-derived glycoprotein hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Several transcription factors cooperate to activate cell-specific and hormone-regulated expression of the gonadotropin beta subunits ( Lhb  and  Fshb ). Among these, NR5A1 (steroidogenic factor 1; SF1) has been shown to directly bind to the  Lhb  promoter, mediate basal and gonadotropin-releasing hormone (GnRH)-stimulated  Lhb  transcription, and possibly directly regulate  Fshb  expression. Recently, the closely-related NR5A2 was shown to activate the rat  Lhb  promoter  in vitro . Here, we further characterized the role of NR5A2 in regulating gonadotropin synthesis. Ectopically expressed NR5A2 directly activated the murine  Lhb  promoter in a manner identical to that of NR5A1, whereas neither factor activated the murine  Fshb  promoter. In LβT2 gonadotrope-like cells, depletion of endogenous NR5A1 or NR5A2 impaired basal and GnRH-stimulated  Lhb  and  Fshb  transcription. To analyze the physiological role of NR5A2 in gonadotropes  in vivo , we generated mice with a gonadotrope-specific deletion of  Nr5a2 . In contrast with our  in vitro  data, these mice had normal pituitary  Lhb  and  Fshb  expression and intact fertility. Together, our data establish that NR5A2 can act in a non-redundant manner to regulate  Lhb  and  Fshb  transcription  in vitro , but is dispensable  in vivo .

NR5A2 Regulates Lhb and Fshb Transcription in Gonadotrope-Like Cells In Vitro, but Is Dispensable for Gonadotropin Synthesis and Fertility In Vivo