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
GLI-similar 3 maintains sexually dimorphic germ cell development in mouse embryos
| Friday, November 08, 2013 — Poster Session IV | |||
|---|---|---|---|
2:00 p.m. – 4:00 p.m. |
FAES Academic Center (Upper-Level Terrace) |
NIEHS |
DEVBIO-11 |
* FARE Award Winner
Authors
- E.K. Ungewitter
- K.N. Lichti-Kaiser
- A.M. Jetten
- H.H-C Yao
Abstract
Germ cells are a uniquely important cell type because they give rise to gametes, the cells responsible for the propagation of all higher species. In the mouse, sexually dimorphic programs of germ cell development begin around embryonic day 13.5, when germ cells in the ovary first express Stra8 and initiate meiosis. This developmental switch is controlled by retinoic acid (RA), which is active in fetal ovaries but silenced in fetal testes due to the presence of the RA-degrading enzyme Cyp26b1. In this study, we set out to uncover new players involved in the dimorphic development of germ cells using mice as a model organism. We found that the zinc finger transcription factor Gli-similar 3 (Glis3) has a testis-specific role in germ cell survival and meiosis. Global Glis3 knockout testes had reduced numbers of germ cells and decreased expression of germ cell markers. Intriguingly, Stra8, the critical regulator of meiotic entry in germ cells, was ectopically elevated in knockout testes despite the fact that neither of its known regulators were changed. These findings reveal a novel role for Glis3 in germ cell survival and meiosis, whereby Glis3 prevents male germ cells from entering meiosis prematurely through a pathway independent of RA.
