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Gonadotropin and kisspeptin gene expression, but not GnRH, are impaired in cFOS deficient mice
Changchuan Xie1, Carrie R Jonak2, Alexander S Kauffman3
1Division of Biomedical Sciences, School of Medicine, University of California, Riverside, CA 92521, USA; Department of Reproductive Medicine, Center for Reproductive Science and Medicine, University of California, San Diego, CA 92093-0674, USA.
Abstract:
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 FSHβ 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 TSHβ 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.
Insights
The transcription factor cFOS is crucial for reproductive function, impacting gonadotropin subunit expression and kisspeptin neuron numbers. Its absence impedes gametogenesis and affects the hypothalamic-pituitary-gonadal axis.
Area of Science:
- Neuroendocrinology
- Molecular Biology
- Reproductive Biology
Background:
- cFOS is a transcription factor that binds to AP1 sites.
- In pituitary gonadotropes, cFOS regulates FSHβ and GnRH receptor genes.
- Its specific role in vivo within the reproductive axis requires elucidation.
Purpose of the Study:
- To investigate the in vivo role of cFOS in reproductive function using cFOS-deficient mice.
- To determine the cell-specific effects of cFOS deficiency on the hypothalamic-pituitary-gonadal axis.
Main Methods:
- Analysis of reproductive parameters in cFOS-deficient mice.
- Assessment of pituitary gonadotropin subunit expression (FSHβ, LHβ, TSHβ).
- Measurement of sex-steroid levels and evaluation of gametogenesis.
- Examination of GnRH and Kiss1 neuron numbers and mRNA levels in the hypothalamus.
Main Results:
- cFOS deficiency impairs gonadotropin subunit expression in the pituitary but spares TSHβ.
- cFOS null mice exhibit normal sex-steroid levels but impeded gametogenesis.
- cFOS is not essential for GnRH neuron development or targeting.
- cFOS deficiency leads to reduced Kiss1 neuron numbers and mRNA levels, particularly in females.
Conclusions:
- cFOS plays a cell-specific role in the reproductive axis.
- It is critical for gonadotrope function and Kisspeptin neuron regulation.
- These findings highlight cFOS's contribution to the control of reproduction.
