| First Author | Xie C | Year | 2015 |
| Journal | Mol Cell Endocrinol | Volume | 411 |
| Pages | 223-31 | PubMed ID | 25958044 |
| Mgi Jnum | J:225928 | Mgi Id | MGI:5694915 |
| Doi | 10.1016/j.mce.2015.04.033 | Citation | Xie C, et al. (2015) Gonadotropin and kisspeptin gene expression, but not GnRH, are impaired in cFOS deficient mice. Mol Cell Endocrinol 411:223-31 |
| abstractText | cFOS is a pleiotropic transcription factor, which binds to the AP1 site in the promoter of target genes. In the pituitary gonadotropes, cFOS mediates induction of FSHbeta and GnRH receptor genes. Herein, we analyzed reproductive function in the cFOS-deficient mice to determine its role in vivo. In the pituitary cFOS is necessary for gonadotropin subunit expression, while TSHbeta is unaffected. Additionally, cFOS null animals have the same sex-steroid levels, although gametogenesis is impeded. In the brain, cFOS is not necessary for GnRH neuronal migration, axon targeting, cell number, or mRNA levels. Conversely, cFOS nulls, particularly females, have decreased Kiss1 neuron numbers and lower Kiss1 mRNA levels. Collectively, our novel findings suggest that cFOS plays a cell-specific role at multiple levels of the hypothalamic-pituitary-gonadal axis, affecting gonadotropes but not thyrotropes in the pituitary, and kisspeptin neurons but not GnRH neurons in the hypothalamus, thereby contributing to the overall control of reproduction. |
