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

Kyle A Wegner, Vatsal Mehta, Jeanette A Johansson, Brett R Mueller, Kimberly P Keil, Lisa L Abler, Paul C Marker, M Mark Taketo, Denis J Headon, Chad M Vezina

Research output: Contribution to journalArticlepeer-review

Abstract

Beta-catenin (CTNNB1) directs ectodermal appendage spacing by activating ectodysplasin A receptor (EDAR) transcription but whether CTNNB1 acts by a similar mechanism in prostate, an endoderm-derived tissue, is unclear. Here we examined the expression, function, and CTNNB1 dependence of the EDAR pathway during prostate development. In situ hybridization studies reveal EDAR pathway components including Wnt10b in 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 Edar and Wnt10b mRNAs. We also used a genetic approach to test the prostatic consequences of activating or inhibiting Edar expression. Edar overexpression does not visibly alter prostatic bud formation or branching morphogenesis, and Edar expression is not necessary for either of these events. However, Edar overexpression is associated with an abnormally thick and collagen-rich stroma in adult mouse prostate. These results support CTNNB1 as a transcriptional activator of Edar and Wnt10b in developing prostate and demonstrate Edar is not only important for ectodermal appendage patterning but also influences collagen organization in adult prostate.

Original languageEnglish
JournalBiology Open
Early online date11 Feb 2019
DOIs
Publication statusE-pub ahead of print - 11 Feb 2019

Keywords

  • Prostate
  • urogenital sinus
  • CTNNB1
  • WNT10B
  • EDAR
  • collagen

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