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While Sertoli cells respond to FSH stimulation, the nature of the response itself varies depending on the developmental status of the animal. Early studies demonstrated that FSH acts as a Sertoli cell mitogen in the prenatal and newborn animal and is instrumental in determining the final spermatogenic capability of the testis. In immature mice, it has been shown that FSH-R signaling appears to be essential for testicular development, the initiation of the first wave of spermatogenesis, and sexual maturity. The critical role played by FSH/FSH-R signaling has been further illustrated through newly uncovered human mutations in the FSHp subunit. Such men display hypogonadism, obstructed pubertal development, small testis size, and azoospermia. Interestingly, mice that lack the FSHp subunit are fertile, as are some Finnish men with an inactivating FSH-R mutation. In both these examples, testis size and sperm production levels are reduced. The development of mice deficient in the FSH receptor (FORKO) provides a model to examine alterations in testicular structure and function in its complete absence. Mutant mice at 2 mo of age have smaller testes, delayed sexual maturity, and reduced fertility. In addition, serum FSH levels are elevated and testosterone levels are reduced amid normal circulating levels of LH. However, details on the structure and functions of the cell type(s) affected in the testis of FORKO mice at early and later ages have not been studied in any detail. This investigation was designed to shed more light on the structural alterations in Sertoli cells of the mutants and their potential impact on functions.