The transcription factor ets variant gene 5 (ETV5; also known as ERM) is essential for self-renewal of spermatogonial stem cells (SSCs). Mice with targeted disruption of Etv5 (Etv5^−/−) undergo the first wave of spermatogenesis, but all SSCs are lost during this time, causing a Sertoli cell-only phenotype. This study examined body and testis growth and the time course of SSC loss in Etv5^−/− mice to understand how loss of ETV5 impacts testicular and somatic development. Body weights were reduced in postnatal Etv5^−/− males, indicating a role of ETV5 in growth. Testis weights and histology in Etv5^−/− and wild-type (WT) males were similar at Postnatal Day 4, but testis weights were reduced at d8 and subsequently, indicating that ETV5 impacts postnatal testis growth. SSC density (SSCs per μm² of seminiferous tubule), estimated using an antibody against GFRA1, was similar in 4d WT and Etv5^−/− mice. By 8 and 12d, GFRA1-positive cell density in Etv5^−/− mice was decreased 17% and 32%, respectively, vs. WT. By 28d, GFRA1-positive cell density in Etv5^−/− was reduced 95%, and GFRA1-positive cells were absent in 36d Etv5^−/− males. In contrast to WT, 35- to 56-day-old Etv5^−/− mice were infertile as assessed by natural breeding, artificial insemination, and in vitro fertilization, although motile sperm were present in epididymides of Etv5^−/− mice during this time. In summary, initial testis development is normal in Etv5^−/− mice despite decreased body weight, but SSC loss begins between 4 and 8d of age, indicating that ETV5 has effects beginning in the early neonatal period. Etv5^−/− mice are infertile even when sperm is produced, indicating that ETV5 loss has other effects besides lack of SSC self-renewal that impair fertility.