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Development ePress online publication date 3 Jul 2008
doi: 10.1242/dev.021493

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Research article

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


Alex C. Kim, Anne L. Reuter, Mohamad Zubair, Tobias Else, Kerri Serecky, Nathan C. Bingham, Gareth G. Lavery, Keith L. Parker, and Gary D. Hammer*
* Author for correspondence (e-mail: ghammer{at}umich.edu)

The nuclear receptor steroidogenic factor 1 (Sf1, Nr5a1) is essential for adrenal development and regulates genes that specify differentiated adrenocortical function. The transcriptional coactivator {beta}-catenin reportedly synergizes with Sf1 to regulate a subset of these target genes; moreover, Wnt family members, signaling via {beta}-catenin, are also implicated in adrenocortical development. To investigate the role of {beta}-catenin in the adrenal cortex, we used two Sf1/Cre transgenes to inactivate conditional {beta}-catenin alleles. Inactivation of {beta}-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 {beta}-catenin inactivation showed decreased proliferation in presumptive adrenocortical precursor cells. By contrast, the Sf1/Crelow transgene effected a lesser degree of {beta}-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 {beta}-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.


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