Delay in sexual maturity of the follicle-stimulating hormone receptor knockout male mouse

In the highly organized and complex process of mammalian spermatogenesis, t he development of an undifferentiated diploid germ cell into a fully differ entiated and mature spermatozoon is orchestrated in a time frame unique for each species including man. If the various hormonal signals including envi ronmental cues that play a critical part in initiating these events are not properly executed, various deficiencies including delay in sexual maturity or puberty are likely. in this study we have followed testicular developme nt and spermatogenesis in the FSH receptor knockout (FORKO) mice from Day 7 onward by using histology and quantitative DNA flow cytometry. The drastic reduction in testicular weight and shrinkage of seminiferous tubules that occurred at this early age persisted into the adult stage in the FORKOs, su ggesting inhibition of the initial developmental processes. The round sperm atids that were clearly abundant on Day 21 in the wild-type and heterozygou s males were few and present only in some tubules of the FORKOs. There were no elongated spermatids in FORKO males on Day 35. The sperm produced by Da y 49 FORKOs were already aberrant, a feature that persisted into adulthood in these animals. As all these changes occurred in a background of normal c irculating testosterone levels, we may conclude that the delay in testicula r development is a consequence of the loss of FSH-receptor signaling. The d elay in sexual maturity of FORKOs was accompanied by reduction in fertility as evidenced by mating studies. Based on these data we suggest that the FO RKO mouse might be a useful experimental model to define the molecular mech anisms that underlie the delay in puberty.