John Nilson Director & Professor, School of Molecular Biosciences School of Molecular Biosciences Washington State University Pullman, WA 99164-4234 Phone: 509-335-9155 Fax: 509-335-9688 Email:jhn@wsu.edu   Ph.D. University of New Mexico ­ Biology, 1976 B.S. University of Tulsa ­ Zoology, 1972 RESEARCH INTERESTS: Reproductive Endocrinology   RESEARCH SUMMARY: Luteinizing hormone (LH) regulates folliculogenesis, ovulation, gametogenesis and gonadal steroidogenesis. Like all members of the glycoprotein hormone family, LH is a heterodimer composed of a common a and unique b subunit. Much of the research in Dr. Nilson’s laboratory focuses on deciphering the critical elements and factors responsible for correct temporal, spatial, and hormonal regulation of the a subunit and LHb genes expressed in pituitary gonadotropes. Current efforts are directed toward establishing higher order genetic pathways that control these gonadotropin genes and other genes that completely define the salient physiological features of gonadotropes. This effort entails extensive gene expression profiling of transgenic mice with DNA microarrays. Dr. Nilson’s laboratory is also interested in using transgenic technology to develop mouse models that mimic human reproductive disorders. Recently, they established a transgenic mouse model where hypersecretion of LH occurs chronically. Female mice are infertile and have several other dire pathological outcomes. Currently, his laboratory is focusing on two of these, pituitary adenomas and granulosa cell (GC) tumors. Both tumorigenic events are preceded by hormone-dependent hyperplasia. They postulate that pituitary adenomas depend on the action of FSH and estrogen whereas GC tumors are triggered by the action of LH, its intracellular mediators, and the altered function of three genes encoding tumor suppressors. Their long-term goal is to identify the complete genetic network necessary and sufficient for the genesis of both tumors. Such a comparative analysis also involves extensive use of DNA microarrays and gene expression profiling and is likely to reveal critical genetic targets common to these and many other tumors. The projects described above are funded by grants from NIDDK (DK28559) and the NCI (CA86387-05). REPRESENTATIVE PUBLICATIONS: Quirk CC, Seachrist DD, Nilson JH. Embryonic expression of the LH beta gene appears to be coupled to the transient appearance of p8, an HMG-related transcription factor. J Biol Chem. 278: 1680-85. 2003 Owens GE, Keri RA, Nilson JH. Ovulatory surges of human CG prevent hormone-induced granulosa cell tumor formation leading to the identification of tumor-associated changes in the transcriptome. Mol Endocrinol. 16:1230-1242. 2002 Jorgensen JS, Nilson JH. AR suppresses transcription of the LHbeta subunit by interacting with steroidogenic factor-1. Mol Endocrinol. 15:1505-1516. 2001 Jorgensen JS, Nilson JH. AR suppresses transcription of the alpha glycoprotein hormone subunit gene through protein-protein interactions with cJun and activation transcription factor 2. Mol Endocrinol. 15:1496-1504. 2001 Quirk CC, Lozada KL, Keri RA, Nilson JH. A single Pitx1 binding site is essential for activity of the LHbeta promoter in transgenic mice. Mol Endocrinol. 15:734-746. 2001