α-Actinin4 nuclear translocation mediates gonadotropin-releasing hormone stimulation of follicle-stimulating hormone β-subunit gene transcription in LβT2 cells

Gonadotropin-releasing hormone (GnRH) regulates the synthesis and secretion of follicle-stimulating hormone (FSH) by stimulating the transcription of Fshβ gene. Our iTRAQ quantitative proteomics result showed that the abundance of α-actinin4 (ACTN4) increased in the nuclei of LβT2 cells upon GnRH induction. Using RNA interference, reverse transcription and real-time PCR, luciferase and transient transfection assays, we proved that ACTN4 is involved in the regulation of mouse Fshβ gene (mFshβ) transcription and its C-terminal calmodulin (CaM)-like domain is crucial for this process. Our study suggests that ACTN4 nuclear translocation mediates GnRH stimulation of mFshβ gene transcription.

► GnRH induces ACTN4 nuclear translocation. ► ACTN4 is involved in the regulation of mFshβ gene transcription. ► C-terminal CaM-like domain of ACTN4 is crucial for the above regulation. ► Both Ca2+ signaling pathway and MAPK pathway play roles in GnRH gene regulation.