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Published on: March 1, 2017
Distinct roles of Bendless in regulating FSC niche competition and daughter cell differentiation
Sumitra Tatapudy1, Jobelle Peralta1, Todd Nystul1
1Department of Anatomy and Department of OB/Gyn-RS, University of California, San Francisco, Center for Reproductive Sciences, Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, 513 Parnassus Avenue, San Francisco, CA, 94143, USA.
Abstract:
A major goal in the study of adult stem cells is to understand how cell fates are specified at the proper time and place to facilitate tissue homeostasis. Here, we found that an E2 ubiquitin ligase, Bendless (Ben), has multiple roles in the Drosophila ovarian epithelial follicle stem cell (FSC) lineage. First, Ben is part of the JNK signaling pathway, and we found that it, as well as other JNK pathway genes, are essential for differentiation of FSC daughter cells. Our data suggest that JNK signaling promotes differentiation by suppressing the activation of the EGFR effector, ERK. Also, we found that loss of ben, but not the JNK kinase hemipterous, resulted in an upregulation of hedgehog signaling, increased proliferation and increased niche competition. Lastly, we demonstrate that the hypercompetition phenotype caused by loss of ben is suppressed by decreasing the rate of proliferation or knockdown of the hedgehog pathway effector, Smoothened (Smo). Taken together, our findings reveal a new layer of regulation in which a single gene influences cell signaling at multiple stages of differentiation in the early FSC lineage.
Insights
The E2 ubiquitin ligase Bendless (Ben) regulates Drosophila follicle stem cell differentiation. Loss of Ben disrupts multiple signaling pathways, impacting stem cell behavior and tissue homeostasis.
Area of Science:
- Developmental Biology
- Stem Cell Biology
- Molecular Genetics
Background:
- Adult stem cells are crucial for tissue homeostasis.
- Understanding stem cell fate specification is a major research goal.
Purpose of the Study:
- To investigate the role of the E2 ubiquitin ligase Bendless (Ben) in the Drosophila ovarian epithelial follicle stem cell (FSC) lineage.
- To elucidate the molecular mechanisms by which Ben regulates stem cell behavior and differentiation.
Main Methods:
- Utilized Drosophila melanogaster as a model organism.
- Investigated gene function through genetic manipulation (loss-of-function).
- Analyzed key signaling pathways including JNK, EGFR/ERK, and Hedgehog.
Main Results:
- Bendless (Ben) is essential for follicle stem cell (FSC) daughter cell differentiation.
- Ben functions within the JNK signaling pathway, suppressing ERK activation to promote differentiation.
- Loss of Ben leads to upregulated Hedgehog signaling, increased proliferation, and enhanced niche competition.
- Phenotypes associated with Ben loss are rescued by reducing proliferation or inhibiting Hedgehog signaling.
Conclusions:
- Bendless (Ben) plays a multifaceted role in regulating stem cell differentiation and behavior.
- Ben integrates multiple signaling pathways (JNK, Hedgehog) to control FSC lineage progression.
- These findings reveal a novel regulatory mechanism impacting stem cell fate and tissue homeostasis.
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