Targeted disruption of β-catenin in Sf1-expressing cells impairs development and maintenance of the adrenal cortex

Author:

Kim Alex C.1,Reuter Anne L.2,Zubair Mohamad2,Else Tobias1,Serecky Kerri1,Bingham Nathan C.2,Lavery Gareth G.2,Parker Keith L.2,Hammer Gary D.1

Affiliation:

1. Department of Medicine, University of Michigan Medical School, Ann Arbor, MI 48109-0678. USA.

2. Departments of Internal Medicine and Pharmacology, UT Southwestern Medical Center, Dallas, TX 75390-8857, USA.

Abstract

The nuclear receptor steroidogenic factor 1 (Sf1, Nr5a1) is essential for adrenal development and regulates genes that specify differentiated adrenocortical function. The transcriptional coactivator β-catenin reportedly synergizes with Sf1 to regulate a subset of these target genes;moreover, Wnt family members, signaling via β-catenin, are also implicated in adrenocortical development. To investigate the role ofβ-catenin in the adrenal cortex, we used two Sf1/Cre transgenes to inactivate conditional β-catenin alleles. Inactivation of β-catenin mediated by Sf1/Crehigh, a transgene expressed at high levels, caused adrenal aplasia in newborn mice. Analysis of fetal adrenal development with Sf1/Crehigh-mediated β-catenin inactivation showed decreased proliferation in presumptive adrenocortical precursor cells. By contrast, the Sf1/Crelow transgene effected a lesser degree of β-catenin inactivation that did not affect all adrenocortical cells, permitting adrenal survival to reveal age-dependent degeneration of the cortex. These results define crucial roles for β-catenin - presumably as part of the Wnt canonical signaling pathway - in both embryonic development of the adrenal cortex and in maintenance of the adult organ.

Publisher

The Company of Biologists

Subject

Developmental Biology,Molecular Biology

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