Specific testicular cellular localization and hormonal regulation of the PKI alpha and PKI beta isoforms of the inhibitor protein of the cAMP-dependent protein kinase

We have previously demonstrated that there exist two distinct genes for the thermostable inhibitor protein of the cAMP-dependent protein kinase, PKI alpha and PKI beta (Van Fatten, S. M., Howard, P., Walsh, D. A., and Maurer, R. A. (1992) Mel. Endocrinol, 6, 2114-2122), We have also shown that in the testis, at least eight forms of PKI beta exist, differing as a result of at least post-translational modification and alternate translational initiation (Kumar, P., Van Fatten, 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 beta being essentially (if not exclusively) a germ cell protein and PKI alpha being expressed primarily in Sertoli cells, Furthermore, there is a progressive change in the forms of PKI beta 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 alpha and PKI beta, The FSH-regulated expression of PKI alpha in the Sertoli cell likely occurs via the normal route of second messenger signal transduction. In contrast, the FSH-dependent PKI beta expression must arise by some form of Sertoli cell-germ cell intercommunication.