Abstract
Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) play critical roles in controlling vertebrate gonadal development and function. Activin, a dimeric growth factor initially identified in the gonads, is important in the differential regulation of the two gonadotropins in mammals. Using goldfish as a model, we have demonstrated that activin stimulates FSHβ but suppresses LHβ expression. The present study demonstrated that the 5′-flanking region of goldfish FSHβ gene is functional in the mouse gonadotrope cell line, LβT2 cells. Similar to its effect on the cultured pituitary cells, activin stimulated FSHβ promoter activity in the LβT2 cells and the effect could be blocked by its binding protein follistatin. Follistatin also significantly suppressed the basal FSHβ promoter activity, suggesting secretion of endogenous activin by the LβT2 cells. Further characterization of the cis-regulatory elements responsible for activin stimulation is now under way in our laboratory.
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