Early development of the gubernaculum and cremaster sac in estrogen receptor knockout mice

Abstract

AIM exogenous estrogen causes gubernacular atrophy and cryptorchidism in fetal rodents. Mice with an estrogen receptor-α (ERα) disrupted gene mutation (αERKO) were studied to determine whether ablation of endogenous estrogen action, through ERα, had an effect on gubernacular development. Serial sagittal sections were made of the pelvis in fetal and day 7 postnatal wild-type and αERKO mice with the estrogen receptor-α“knockout” gene mutation. Wild-type ( n=24), heterozygote ( n=13) and αERKO mice ( n=12) were sacrificed at 16, 17 and 18 days fetal life and at 7 days postnatally. The size of the gubernaculum, cremaster muscle, cremaster sac, and the width of the sac at both ends in day 7 mice were quantitated by computer analysis. Visually and statistically the ERKO mice could not be separated from the wild-type mice during fetal life. At day 7 postnatally, a thicker cremaster sac was noted morphologically, and also a statistically significant difference was seen in the width of the cremaster sac at the sac's tip. Sac area, cremaster muscle area and the width of the sac at the sac's end did not differ significantly. Overall there is minimal phenotypic change observed in the αERKO mouse compared to wild-type at the early developmental stages investigated. However, at postnatal day 7, there is a difference in the width of the cremasteric sac tip. This suggests that the effect of ERα, and thus signaling on the developing gubernaculum, occurs late in development. Alternatively, an action from the recently discovered ERβ may be involved. Exploration of a βERKO and the double knock-out αERKO/βERKO mouse should be informative in evaluating the effect of endogenous estrogens in gubernacular development.