Edar is a downstream target of beta-catenin and drives collagen accumulation in the mouse prostate

Beta-catenin (CTNNB1) directs ectodermal appendage spacing by activating ectodysplasin A receptor (EDAR) transcription, but whether CTNNB1 acts by a similar mechanism in the prostate, an endoderm-derived tissue, is unclear. Here we examined the expression, function, and CTNNB1 dependence of the EDAR pathway during prostate development. hybridization studies reveal EDAR pathway components including in the developing prostate and localize these factors to prostatic bud epithelium where CTNNB1 target genes are co-expressed. We used a genetic approach to ectopically activate CTNNB1 in developing mouse prostate and observed focal increases in and mRNAs. We also used a genetic approach to test the prostatic consequences of activating or inhibiting expression. overexpression does not visibly alter prostatic bud formation or branching morphogenesis, and expression is not necessary for either of these events. However, overexpression is associated with an abnormally thick and collagen-rich stroma in adult mouse prostates. These results support CTNNB1 as a transcriptional activator of and in the developing prostate and demonstrate is not only important for ectodermal appendage patterning but also influences collagen organization in adult prostates.This article has an associated First Person interview with the first author of the paper.