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Volume 272, Number 32, Issue of August 8, 1997 pp. 20021-20029
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Specific Testicular Cellular Localization and Hormonal Regulation of the PKI and PKI Isoforms of the Inhibitor Protein of the cAMP-dependent Protein Kinase

(Received for publication, March 6, 1997, and in revised form, May 19, 1997)

Scott M. Van Patten , Lucy F. Donaldson , Michael P. McGuinness ^§ , Priyadarsini Kumar , Azita Alizadeh , Michael D. Griswold ^§ and Donal A. Walsh

From the  Department of Biological Chemistry, School of Medicine, University of California, Davis, California 95616 and the ^§ Department of Biochemistry and Biophysics, Washington State University, Pullman, Washington 99164

We have previously demonstrated that there exist two distinct genes for the thermostable inhibitor protein of the cAMP-dependent protein kinase, PKI and PKI (Van Patten, S. M., Howard, P., Walsh, D. A., and Maurer, R. A. (1992) Mol. Endocrinol. 6, 2114-2122). We have also shown that in the testis, at least eight forms of PKI exist, differing as a result of at least post-translational modification and alternate translational initiation (Kumar, P., Van Patten, S. M., and Walsh, D. A. (1997) J. Biol. Chem. 272, 20011-20020). We now report that in the testis, there is a unique cellular distribution of protein kinase inhibitor forms, with PKI being essentially (if not exclusively) a germ cell protein and PKI being expressed primarily in Sertoli cells. Furthermore, there is a progressive change in the forms of PKI that are present within germ cells with development that is initiated in testis tubules and continues as the germ cells migrate through the epididymis. These conclusions are derived from studies with isolated cell populations and with the at/at germ cell-deficient mouse line, by in situ hybridization, and by following the developmental expression of these proteins in both testis and epididymis. We have also shown that follicle-stimulating hormone (FSH) can increase the expression of both PKI and PKI. The FSH-regulated expression of PKI in the Sertoli cell likely occurs via the normal route of second messenger signal transduction. In contrast, the FSH-dependent PKI expression must arise by some form of Sertoli cell-germ cell intercommunication.

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