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Genetic Factors Contributing to Defective Spermatogonial Differentiation in Juvenile Spermatogonial Depletion (Utp14b^jsd) Mice¹

Department of Experimental Radiation Oncology,⁴ The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030 Department of Agricultural and Environmental Sciences and George Washington Carver Experiment Station,⁵ Tuskegee University, Tuskegee, Alabama 36088 Department of Morphology,⁶ Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil 31270-901 Department of Obstetrics and Gynecology,⁷ Baylor College of Medicine, Houston, Texas 77030

ABSTRACT

Male mice that are homozygous for the juvenile spermatogonial depletion (jsd) mutation in the Utp14b gene undergo several waves of spermatogenesis. However, spermatogonial differentiation ceases and in adults, spermatogonia are the only germ cells that remain. To understand further the blockage in spermatogonial differentiation in Utp14b^jsd mutant mice, we correlated the rate and severity of spermatogonial depletion and the restoration of spermatogenesis following the suppression of testosterone or elevation of testicular temperature with the genetic background. Testes from Utp14b^jsd mutant mice on B6, C3H, and mixed C3H-B6–129 (HB129) genetic backgrounds all showed steady decreases in the numbers of normal spermatogonia between 8 wk and 20 wk of age. The percentages of tubules with differentiating germ cells were higher and the spermatogonia were more advanced in C3H- background than in B6- or HB129-background Utp14b^jsd mice. Genetic crosses showed that the source of the Y chromosome was a major factor in determining the severity of spermatogonial depletion in Utp14b^jsd mutant mice. When Utp14b^jsd mutants were subjected to total androgen ablation or unilateral cryptorchidization, spermatogenic development recovered markedly in the C3H and HB129 background but showed less recovery in the B6-background mice. The differences noted between the strains in terms of the severity of spermatogonial depletion were not dependent upon testosterone level or scrotal temperature but correlated with the magnitudes of the effects of elevated temperature on normal and Utp14b^jsd mutant spermatogenic cells. Thus, the abilities of germ cells in certain strains to survive elevated temperatures may be related to their abilities to maintain some degree of differentiation potential after the Utp14b^jsd gene is mutated.

high-resolution light microscopy,, jsd mutation,, spermatogenesis,, spermatogonia,, testis,, testosterone,, Y chromosome

³Current address: Department of Medicine, Medical College of Georgia, Augusta, GA 30912.

¹Support provided by the National Institutes of Health (R01 HD-40397, Cancer Center Support Grant CA-16672, and Training Grant T32 HD-07324), Fundacao de Amparo a Pesquisa do Estado de Minas Gerais (FAPEMIG; CBB-1815/05), and a Research Fellowship to H.C-G. from the Brazilian Research Council (CNPq 307172/2003-1).

Correspondence: ²Marvin L. Meistrich, University of Texas M. D. Anderson Cancer Center, Department of Experimental Radiation Oncology, 1515 Holcombe Boulevard, Box 66, Houston, TX 77030. FAX: 713 794 5369; e-mail: meistrich{at}mdanderson.org