Molecular genetic analysis of glucocorticoid signalling in development

J Steroid Biochem Mol Biol. 1995 Jun;53(1-6):33-5. doi: 10.1016/0960-0760(95)00038-2.


A null mutation of the glucocorticoid receptor was generated by homologous recombination. Mutant newborn mice showed impaired lung development, hypertrophy of the adrenal cortex and a strongly reduced size of the adrenal medulla. Phenylethanolamine N-methyltransferase (PNMT) was undetectable in the adrenals of the mutant mice. Serum levels of corticosterone were moderately and ACTH levels were strongly elevated in the mutants. A weaker but significant increase of corticosterone and ACTH was observed already in heterozygous animals. This points to a dysregulation of the HPA axis due to defective feedback regulation via the glucocorticoid receptor. Liver gluconeogenetic enzymes were reduced to a variable degree. Whereas survival of heterozygous mutants was not affected, most of the homozygous mutant mice died during the perinatal period.

Publication types

  • Review

MeSH terms

  • Animals
  • Gene Expression Regulation, Developmental*
  • Glucocorticoids / physiology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Receptors, Glucocorticoid / physiology*


  • Glucocorticoids
  • Receptors, Glucocorticoid