October 9 - 12, 2012
Building 10 & Natcher Conference Center
- General Schedule of Events
- Opening Plenary Session
- Concurrent Symposia Sessions
- Poster Sessions
- National Graduate Student Research Conference
- FARE Award Ceremony
- Special Exhibits on Resources for Intramural Research
- TSA Research Festival Exhibit Show
- Clinical Center Tours
- Research Festival Committees
- Past Research Festivals
COUP-TFII: a new player in the dimorphic establishment of the male and female reproductive tracts in the mouse embryo
| Friday, November 08, 2013 — Poster Session IV | |||
|---|---|---|---|
2:00 p.m. – 4:00 p.m. |
FAES Academic Center (Upper-Level Terrace) |
NIEHS |
DEVBIO-3 |
Authors
- H.L. Franco
- M.-J. Tsai
- S.Y. Tsai.
- H.HC Yao
Abstract
Disorders of sexual development occur in 1/4500 births with a majority affecting the reproductive tracts (RT). RT development depends on the regression and differentiation of two primitive mesonephric ducts into a single RT. This process is controlled by two hormones: androgens and anti-Müllerian hormone (AMH). Chicken ovalbumin upstream promoter transcription factor II (COUP-TFII) regulates adult RT function and is expressed in the mesenchyme of the embryonic gonad and mesonephros. To determine its role in RT development, COUP-TFII was ablated in the embryonic gonad and mesonephros. Surprisingly, this ablation resulted in the presence of two RTs in both males and females making this the first model where a genetic alteration caused a failure of ductal regression in both sexes. Insufficient AMH production by the knockout testes could cause female duct retention; however, AMH expression was similar to controls. Ectopic androgen production could maintain the male duct; however, the knockout ovaries did not display ectopic androgen-producing cells. Together, these data indicate that COUP-TFII mediates ductal regression by a mechanism other than gonadal hormone production and suggests that mesonephric mesenchymal COUP-TFII signals ductal epithelial cell regression. Understanding this novel mechanism may provide new insight into the etiology of disorders of sexual development.
