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 fo r the thermostable inhibitor protein of the cAMP-dependent protein kin ase, 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 a lso 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 th at in the testis, there is a unique cellular distribution of protein k inase inhibitor forms, with PKI beta being essentially (if not exclusi vely) a germ cell protein and PKI alpha being expressed primarily in S ertoli cells, Furthermore, there is a progressive change in the forms of PKI beta that are present within germ cells with development that i s initiated in testis tubules and continues as the germ cells migrate through the epididymis, These conclusions are derived from studies wit h isolated cell populations and with the at/at germ cell-deficient mou se line, by in situ hybridization, and by following the developmental expression of these proteins in both testis and epididymis, We have al so shown that follicle-stimulating hormone (FSH) can increase the expr ession 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 s econd messenger signal transduction. In contrast, the FSH-dependent PK I beta expression must arise by some form of Sertoli cell-germ cell in tercommunication.