Abstract
The role of insulin 3-like (Insl3) hormone signaling in the testicular descent process has been demonstrated. The purpose of the present study was to evaluate epididymal development in Insl3-deficient mice. Heterozygous and homozygous Insl3 mutants of a mixed CD1 X 129/Sv genetic background were generated by breeding Insl3-/- females with Insl3+/- males, and their genotypes were determined by polymerase chain reaction. On the first postnatal day, newborn males were sacrificed, embedded in paraffin, and cut in 4 mm sections. Sections were stained with hematoxylin/eosin and immunoreacted with anti-alpha actin antibody. An analysis of stained sections indicated an arrest in the development of the epididymis in all homozygous mice. The cauda and corpus of the epididymis were undersized. Compared to the heterozygous epididymis, the homozygous epididymis had fewer peritubular layers and dwarfish musculature. We confirmed this with immunostaining with monoclonal antibodies against alpha-smooth muscle actin. Defective development of the smooth musculature in the epididymis of Insl3 homozygous mutant mice, combined with its high intraabdominal undescended position, supports previous observations regarding the importance of intact epididymis morphology and function for descent of the epididymo-testicular unit.
Highlights
During early embryonic development of the urogenital tract, mesentery connects the gonads and the Wollfian and Müllerian ducts to the abdominal wall
The mechanism controlling testicular descent in mice was determined by analyzing mouse lines that lack insulin-like 3 (Insl3) hormone and its receptor, Lgr8/Great [3]
These findings clearly demonstrate the role of Insl3 signaling in the process of testicular descent
Summary
During early embryonic development of the urogenital tract, mesentery connects the gonads and the Wollfian and Müllerian ducts to the abdominal wall. During male and female development, two parts of the genital mesentery, the cranial suspensory ligament and the caudal genital ligament gubernaculums, are believed to be responsible for sexual dimorphism in the position of testis and ovary [1]. The mechanism controlling testicular descent in mice was determined by analyzing mouse lines that lack insulin-like 3 (Insl3) hormone and its receptor, Lgr8/Great [3]. Bilateral cryptorchidism in Insl3- and Lgr8- deficient mice is due to impaired development of the gubernaculum [4,5]. These findings clearly demonstrate the role of Insl signaling in the process of testicular descent
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