Late onset of spermatogenesis and gain of fertility in POG-deficient mice indicate that POG is not necessary for the proliferation of spermatogonia

The germ cell-deficient (gcd) mouse mutation is a recessive, transgenic insertional mutation associated with the disruption of two Chr11 genes, Pog (proliferation of germ cells) and Vrk2 (vaccinia virus-related protein kinase 2). We have recently shown that like gcd/gcd mice, targeted Pog2/2 males and fe-males show virtually no spermatogenesis or oogenesis at 4–6 wk of age. Because Pog is deleted in gcd/gcd and Pog2/2 mice, a comparison of the phenotypes of the two mouse models is ap-propriate. Here, we report that unlike in POG-deficient females, the germ cells in POG-deficient males eventually populate the seminiferous tubules at 9 wk, and fertility can be achieved by 12 wk. Homozygous gcd/gcd males did not show a similar de-gree of germ cell population, and most gcd/gcd males remained infertile at 16 and 22 wk of age. A comparison of the degree of germ cell deficiency at 13.5 days postcoitum and 1 day post-partum between Pog2/2 and gcd/gcd males revealed that gcd/ gcd males had far fewer germ cells than Pog2/2 males at both time points. Our data suggest that Pog is essential for proper primordial germ cell proliferation in the embryonic stage but is not needed for spermatogonial proliferation after birth. Thus, the difference in the spermatogenetic potential in adult Pog2/2 and gcd/gcd mice may result from the severity of germ cell de-ficiency rather than from the inability of gcd/gcd spermatogonia to proliferate efficiently. The greater deficiency of germ cells before the onset of spermatogenesis seen in gcd/gcd males com-pared to Pog2/2 mice suggests either that the different back-ground affects the outcome of Pog deletion or that Vrk2 has additional effects on germ cell development. developmental biology, gametogenesis, sperm, spermatogenesis, testi