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¹ Department of Neurobiology and Physiology, Northwestern University, 2205 Tech Drive, Evanston, Illinois 60208, USA
² Department of Medicine, Northwestern Medical School, Chicago, Illinois 60611, USA

(Requests for offprints should be addressed to T K Woodruff; Email: tkw{at}northwestern.edu)

Members of the transforming growth factor-ß (TGFß) family control diverse cellular responses including differentiation, proliferation, controlled cell death and migration. The response of a cell to an individual ligand is highly restricted yet the signaling pathways for TGFß, activin and bone morphogenic proteins share a limited number of receptors and activate similar intracellular cytoplasmic co-regulators, Smads. A central question in the study of this family of ligands is how cells titrate and integrate each TGFß-like signal in order to respond in a cell- and ligand-specific manner. This study uses the pituitary gonadotrope cell line, LßT2, as a model to delineate the relative contribution of TGFß and activin ligands to follicle-stimulating hormone (FSH) biosynthesis. It was found that pituitary gonadotrope cells do not express the TGFß type II (TßRII) receptor and are therefore not responsive to the TGFß ligand. Transfection of the receptor restores TGFß signaling capabilities and the TGFß-mediated stimulation of FSHß gene transcription in LßT2 cells. Consequently, we evaluated the presence of the TßRII in the adult mouse pituitary. TßRII does not co-localize with FSH-producing cells; however it is detected on the cell surface of prolactin- and growth hormone-positive cells. Taken together, these results suggest that the bioavailability of the TGFß-specific receptor rather than TGFß dictates pituitary gonadotrope selectivity to activin, which is necessary to maintain normal reproductive function. It is likely that the ligand-restricted mechanisms employed by the gonadotrope are present in other cells, which could explain the distinct control of many cellular processes by members of the TGFß superfamily.

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