We just published a paper in Endocrinology entitled Sexually Dimorphic Regulation of Gonadotrope Cell Hyperplasia in Medaka Pituitary via Mitosis and Transdifferentiation. This paper is based on my PhD student Muhammad Rahmad Royan with the help of our collaborator in Japan, Daichi Kayo.
In this paper, we show that in the fish pituitary, the proliferation of the endocrine cells regulating reproduction are differentially regulated in males and females. We demonstrate the existence of an interesting phenomenon, the phenotypic change of Tsh cells into Fsh cells in females only.
Abstract: The 2 pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), regulate the reproductive function in all vertebrates. While many studies have investigated the regulation of gonadotropin production and release by sex steroid feedback, its role on the regulation of gonadotrope cell number remains unclear. Using medaka as a model and an optimized protocol to restore physiological sex steroids levels following gonadectomy, we show that gonadal sex steroids not only decrease fshb transcript levels, but also Fsh cell number in both sexes. We then investigated the origin of Fsh cell hyperplasia induced by gonadectomy. In both sexes, bromodeoxyuridine incubation shows that this is achieved via Fsh cell mitosis. In situ hybridization reveals that new Fsh cells also originate from transdifferentiating Tsh cells in females, but not in males. Both phenomena are inhibited by sex steroid supplementation via feeding. In males (but not females), gonadectomy (without recovery with sex steroid supplementation) also reduces sox2 transcript levels and Sox2-immunopositive population size, suggesting that Sox2 progenitors may be recruited to produce new Fsh cells. Opposite to Fsh cells, gonadectomy decreases lhb levels in both sexes, and levels are not restored by sex steroid supplementation. In addition, the regulation of Lh cell number also seems to be sex dependent. Removal of gonadal sex steroids stimulates Lh cell mitosis in male (like Fsh cells) but not in females. To conclude, our study provides the first evidence on sexually dimorphic mechanisms used in the fish pituitary to remodel gonadotrope populations in response to sex steroids.
More info on the study in the open access publication : https://doi.org/10.1210/endocr/bqad030