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PPP1CC2, one of four isoforms of the ser/thr protein phosphatase PP1, is a mammalian-specific splice variant of the  Ppp1cc  gene, and the only isoform whose expression is confined almost completely to spermatogenic cells. Additionally, PPP1CC2 is the sole isoform found in mammalian spermatozoa. Although PPP1CC1, the other  Ppp1cc  product, is expressed in many tissues including testis, the only phenotype resulting from deletion of  Ppp1cc  gene is male infertility. To determine which of the products of  Ppp1cc  is essential for male fertility, we created two PPP1CC2 transgenes, eTg-G2 and pTg-G2, where  Ppp1cc2  expression was driven by the putative endogenous promoter of  Ppp1cc  or by the testis specific human  Pgk2  promoter, respectively. Our results demonstrate that the 2.6-kb genomic region directly upstream of the  Ppp1cc  structural gene can drive expression of  Ppp1cc2,  and recapitulate the wild-type tissue specificity of PPP1CC2 in transgenic mice. More importantly, we show that expression of PPP1CC2 alone, via either promoter, is able not only to restore normal spermatogenesis, but the fertility of  Ppp1cc  null mice as well, provided that transgenic PPP1CC2 expression in testis reaches at least a lower threshold level equivalent to approximately 50% of its expression by a  Ppp1cc +/−  male. We conclude that the endogenous  Ppp1cc  promoter normally functions in the testis to maintain a sufficient level of PPP1CC2 expression for normal spermatogenesis to occur, and that production of spermatozoa capable of fertilization in vivo can take place in the complete absence of PPP1CC1 expression.

Significant Expression Levels of Transgenic PPP1CC2 in Testis and Sperm Are Required to Overcome the Male Infertility Phenotype of Ppp1cc Null Mice