Molecular genetic analysis of glucocorticoid signalling in development

doi:10.1016/0960-0760(95)00038-2

The Journal of Steroid Biochemistry and Molecular Biology

Volume 53, Issues 1–6, June 1995, Pages 33-35

https://doi.org/10.1016/0960-0760(95)00038-2 Get rights and content

Abstract

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.

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Molecular genetic analysis of glucocorticoid signalling in development

Abstract

Cell

Neuron

Neuron

Cell

Cell

Neuron

A DNA sequence of 15 base pairs is sufficient to mediate both glucocorticoid and progesterone induction of gene expression