Transabdominal testicular descent is disrupted in mice with deletion of insulinlike factor 3 receptor

J Pediatr Surg. 2003 Dec;38(12):1793-8. doi: 10.1016/j.jpedsurg.2003.08.047.


Background: Several factors are implicated in transabdominal testicular descent, including insulinlike factor 3 (INSL3) hormone and Müllerian-inhibiting substance (MIS). A transgene insertional mutation found on chromosome 5 in the mouse, known as crsp, causes deletion of a transmembrane G protein-coupled receptor gene, Great, which is highly expressed in the gubernaculum. The authors describe here a detailed analysis of the testicular descent and gubernacular development in crsp mice to determine the role of the Great gene in this process.

Methods: Homozygous (crsp/crsp) mutant and wild-type heterozygous (crsp/+) mice were examined at birth (D 0) and at days 10 (D 10) and 30 (D 30) postnatally. Serial sagittal or coronal sections were analyzed for position of the gonads and cremaster sac development.

Results: Transabdominal testicular descent was absent at D 0 in crsp/crsp homozygous mice with no swelling reaction in the gubernacula. By D 10 the cremaster sac was significantly thinner (P <.05) and contained less collagen in the mutants than in the wild-type controls. On D 30 the cremaster sacs of mutant males were similar in thickness to those in females.

Conclusions: Disruption of the Great gene causes failure of the transabdominal phase of descent, identical to that seen in the Insl3-deficient mutants, consistent with the recent data suggesting that Great gene encodes the Insl3 transmembrane receptor. No differences between D 30 mutant males and females were found in the gubernacula, suggesting that Insl3/Great signaling regulates gubernacular development.

MeSH terms

  • Animals
  • Animals, Newborn
  • Chromosomes, Mammalian
  • Cryptorchidism / genetics*
  • Gene Deletion*
  • Insulin
  • Ligaments
  • Male
  • Mice
  • Mice, Mutant Strains
  • Mutagenesis, Insertional
  • Mutation
  • Proteins / genetics*
  • Receptors, G-Protein-Coupled / genetics*
  • Transgenes


  • Insulin
  • Leydig insulin-like protein
  • Proteins
  • Receptors, G-Protein-Coupled