Journal
CELL REPORTS
Volume 7, Issue 3, Pages 722-734Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2014.04.025
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Funding
- California Institute for Regenerative Medicine to the University of California, San Diego
- Damon Runyon Cancer Research Foundation and the UCSD IRACDA program
- Portuguese Foundation for Science and Technology [SFRH/BD/33253/2007]
- Ellison Medical Foundation
- Emerald Foundation
- Charitable Foundation
- American Cancer Society
- NIH
- NHMRC
- Australian Drosophila Biomedical Research
- NIH [GM080501, CA14915, CA80100]
- National Institute of General Medical Sciences [8P41GM103533-17]
- National Center for Research Resources [5P41RR011823-17]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/33253/2007] Funding Source: FCT
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Stem cells reside within specialized microenvironments, or niches, that control many aspects of stem cell behavior. Somatic hub cells in the Drosophila testis regulate the behavior of cyst stem cells (CySCs) and germline stem cells (GSCs) and are a primary component of the testis stem cell niche. The shutoff (shof) mutation, characterized by premature loss of GSCs and CySCs, was mapped to a locus encoding the evolutionarily conserved transcription factor Escargot (Esg). Hub cells depleted of Esg acquire CySC characteristics and differentiate as cyst cells, resulting in complete loss of hub cells and eventually CySCs and GSCs, similar to the shof mutant phenotype. We identified Esg-interacting proteins and demonstrate an interaction between Esg and the corepressor C-terminal binding protein (CtBP), which was also required for maintenance of hub cell fate. Our results indicate that niche cells can acquire stem cell properties upon removal of a single transcription factor in vivo.
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