期刊
DEVELOPMENTAL CELL
卷 27, 期 1, 页码 5-18出版社
CELL PRESS
DOI: 10.1016/j.devcel.2013.09.003
关键词
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资金
- Association pour la Recherche sur lea Cancers [SL220120605297]
- ANR (ADSTEM)
- Fondation de la Recherche Medicale (FRM) [DEQ20090515425]
- Boehringer Ingelheim Foundation
- ARC
- ANR [ANR08-GENOPAT-002]
- Association for International Cancer Research (AICR)
- Medical Research Council (MRC)
Adrenal glands and gonads share a common primordium (AGP), but the molecular events driving differentiation are poorly understood. Here we demonstrate that the Wilms tumor suppressor WT1 is a key factor defining AGP identity by inhibiting the steroidogenic differentiation process. Indeed, ectopic expression of WT1 precludes differentiation into adrenocortical steroidogenic cells by locking them into a progenitor state. Chromatin immunoprecipitation experiments identify Tcf21 and Gill as direct targets of WT1. Moreover, cell lineage tracing analyses identify a long-living progenitor population within the adrenal gland, characterized by the expression of WT1, GATA4, GLI1, and TCF21, that can generate steroidogenic cells in vivo. Strikingly, gonadectomy dramatically activates these WT1(+) cells and leads to their differentiation into gonadal steroidogenic tissue. Thus, our data describe a mechanism of response to organ loss by recreating hormone-producing cells at a heterotopic site.
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