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This Article Full Text Full Text (PDF) All Versions of this Article: 69/1/161    most recent biolreprod.102.014654v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lu, B. Articles by Bishop, C. E. Search for Related Content PubMed PubMed Citation Articles by Lu, B. Articles by Bishop, C. E. Agricola Articles by Lu, B. Articles by Bishop, C. E.

Late Onset of Spermatogenesis and Gain of Fertility in POG-Deficient Mice Indicate that POG Is Not Necessary for the Proliferation of Spermatogonia¹

Department of Obstetrics and Gynecology,⁴ Baylor College of Medicine, Houston, Texas 77030 Department of Molecular and Human Genetics,⁵ Baylor College of Medicine, Houston, Texas 77030

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 Pog^-/- males and females show virtually no spermatogenesis or oogenesis at 4–6 wk of age. Because Pog is deleted in gcd/gcd and Pog^-/- mice, a comparison of the phenotypes of the two mouse models is appropriate. 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 degree 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 postpartum between Pog^-/- and gcd/gcd males revealed that gcd/gcd males had far fewer germ cells than Pog^-/- 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 Pog^-/- and gcd/gcd mice may result from the severity of germ cell deficiency 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 compared to Pog^-/- mice suggests either that the different background affects the outcome of Pog deletion or that Vrk2 has additional effects on germ cell development.

¹ Supported by grants from the NIH to C.E.B.

² Correspondence: Colin E. Bishop, Department of Obstetrics & Gynecology, Baylor College of Medicine, 6550 Fannin Street (#880), Houston, TX 77030. FAX: 713 798 5074; bishop{at}bcm.tmc.edu

³ Current address: Beijing Institute of Biotechnology, Beijing, China, 100071