The germ cell-deficient (gcd) mutation is a recessive transgenic insertional mutation leading to a deficiency of primordial germ cells (PGCs). We have recently shown that the gene underlying this mutation is Pog, which is necessary for normal proliferation of PGCs. Here we show that Pog is also involved in spermatogenesis in that meiosis is impaired in Pog-deficient mice. Yeast two-hybrid screening revealed that POG interacted with GGN1 and GGN3, two proteins formed by alternate splicing of the same gene, gametogenetin (Ggn). Ggn had more than 10 different splice variants giving rise to three proteins, GGN1, GGN2, and GGN3. The three proteins had different subcellular localizations, with GGN1, GGN2, and GGN3 localized along the nuclear membrane, in the cytoplasm, and in the nucleus/nucleoli respectively. The expression of Ggn was confined to late pachytene spermatocytes and round spermatids, a time window concomitant with the occurrence of meiosis. Mouse Ggn and Pog were both expressed in primary spermatocytes. Co-expression of POG with GGN1 or GGN3 in HeLa cells changed the localization of POG to the perinuclear localization or the nucleoli, respectively. Our data showed that in addition to functioning in proliferation of primordial germ cells, POG also functioned in spermatogenesis. Two spatial and temporal regulated proteins, GGN1 and GGN3, interacted with POG, regulated the localization of POG, and played a role in spermatogenesis.