Skip to main content
. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Mol Cell Endocrinol. 2020 Oct 12;519:111043. doi: 10.1016/j.mce.2020.111043

Figure 3. Antagonism between Wnt/β-catenin and cAMP/PKA signaling helps determine adrenocortical cell fate.

Figure 3.

Activation of Wnt/β-catenin signaling induces a transcriptional program that promotes zG differentiation, which includes several genes that support the production of aldosterone (e.x. Agtr1, Cyp11b2, Nr4a1, and Nr4a2). Simultaneously, Wnt/β-catenin activation represses zF identity through mechanisms that include direct up regulation of Pde2a. Conversely, cAMP/PKA signaling promotes zF differentiation by increasing expression of several genes that support the production of glucocorticoids (e.x. Mc2r, Cyp11b1, Star, Cyp11a1, and Akr1b7). PKA signaling additionally represses Wnt/β-catenin activation through mechanisms that include inhibition of Wnt4. The balance between Wnt and PKA signaling in part determines adrenocortical cell fate. Schematic created with BioRender.com.