Figure 4.

Underlying mechanism for AMH inhibition by androgens in the pubertal Sertoli cell. (A) Sertoli cells produce high levels of AMH during the prenatal and prepubertal period. This high expression is a direct consequence of SF1, GATA4 and WT1 interaction with their own binding sites on the AMH promoter and also of protein-protein interactions with each other. (B) At pubertal onset, Sertoli cells express the androgen receptor (AR) and can respond to androgen action. Androgens inhibit AMH promoter activity through the AR. Inhibition could be due either to a direct interaction between the ligand-bound AR and the SF1 sites present on the AMH promoter (blockage by competition), or due to a protein-protein interaction between the ligand-bound AR and promoter-bound SF1 (blockage by interaction). In either scenario, the ligand-bound AR prevents SF1 from exerting its stimulatory effect on AMH promoter activity, thus resulting in a decrease in AMH expression. Based on ref. [30].