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Updated: Jul 17, 2026

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
Published on: July 25, 2017
The Drosophila tumor suppressors Expanded and Merlin differentially regulate cell cycle exit, apoptosis, and Wingless
Brett J Pellock1, Eugene Buff, Kristin White
1Massachusetts General Hospital Cutaneous Biology Research Center, Charlestown, MA 02129, and University of California, Berkeley, Department of Molecular and Cell Biology 94720, USA.
Abstract:
Mutations that inactivate either merlin (mer) or expanded (ex) result in increased cell growth and proliferation in Drosophila. Both Mer and Ex are members of the Band 4.1 protein superfamily, and, based on analyses of mer ex double mutants, they are proposed to function together in at least a partially redundant manner upstream of the Hippo (Hpo) and Warts (Wts) proteins to regulate cell growth and division. By individually analyzing ex and mer mutant phenotypes, we have found important qualitative and quantitative differences in the ways Mer and Ex function to regulate cell proliferation and cell survival. Though both mer and ex restrict cell and tissue growth, ex clones exhibit delayed cell cycle exit in the developing eye, while mer clones do not. Conversely, loss of mer substantially compromises normal developmental apoptosis in the pupal retina, while loss of ex has only mild effects. Finally, ex has a role in regulating Wingless protein levels in the eye that is not obviously shared by either mer or hpo. Taken together, our data suggest that Mer and Ex differentially regulate multiple downstream pathways.
Insights
Mutations in merlin (mer) and expanded (ex) genes impact Drosophila cell growth. These proteins, part of the Band 4.1 superfamily, differentially regulate cell proliferation, survival, and Wingless signaling.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Merlin (mer) and expanded (ex) are Band 4.1 superfamily proteins implicated in regulating cell growth and proliferation in Drosophila.
- Previous studies suggested mer and ex function redundantly upstream of the Hippo (Hpo) and Warts (Wts) pathway.
Purpose of the Study:
- To investigate the distinct roles of merlin and expanded in regulating cell proliferation, survival, and downstream signaling pathways.
- To elucidate the differential functions of mer and ex beyond their proposed redundant roles.
Main Methods:
- Analysis of individual mer and ex mutant phenotypes in Drosophila.
- Examination of cell cycle progression and apoptosis in developing eye and pupal retina.
- Assessment of Wingless protein levels in the eye.
Main Results:
- Both mer and ex mutations lead to increased cell growth, but exhibit distinct effects on cell cycle exit and apoptosis.
- ex mutant clones show delayed cell cycle exit in the eye, while mer mutant clones do not.
- Loss of mer significantly impairs developmental apoptosis, whereas loss of ex has a milder effect.
- ex, but not mer or hpo, plays a role in regulating Wingless protein levels in the eye.
Conclusions:
- Merlin and expanded proteins play distinct, non-redundant roles in regulating cell proliferation and survival.
- These proteins differentially modulate downstream pathways, including Wingless signaling.
- The findings highlight the complex regulatory network governing cell growth and division in Drosophila.
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