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Updated: May 2, 2026
Live-imaging of the Drosophila Pupal Eye
Published on: January 12, 2015
Drosophila USP5 controls the activation of apoptosis and the Jun N-terminal kinase pathway during eye development
Xiaolan Fan1, Qinzhu Huang1, Xiaolei Ye1
1School of Optometry and Ophthalmology and Eye Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Abstract:
The Jun N-terminal kinase pathway plays an important role in inducing programmed cell death (apoptosis) and is activated in a variety of contexts. The deubiquitinating enzymes (DUBs) are proteases regulating the protein stability by ubiquitin-proteasome system. Here, for the first time, we report the phenotypes observed during eye development that are induced by deleting Drosophila USP5 gene, which encodes one of the USP subfamily of DUBs. usp5 mutants displayed defects in photoreceptor differentiation. Using genetic epistasis analysis and molecular markers, we show that most of these phenotypes are caused by the activation of apoptosis and JNK pathway. These data may provide a mechanistic model for understanding the mammalian usp5 gene.
Insights
Deleting the Drosophila USP5 gene disrupts eye development by activating programmed cell death (apoptosis) and the Jun N-terminal kinase (JNK) pathway, impacting photoreceptor differentiation.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- The Jun N-terminal kinase (JNK) pathway is crucial for programmed cell death (apoptosis).
- Deubiquitinating enzymes (DUBs) regulate protein stability via the ubiquitin-proteasome system.
Purpose of the Study:
- To investigate the function of the Drosophila USP5 gene, a deubiquitinating enzyme, during eye development.
- To elucidate the molecular mechanisms underlying USP5's role in photoreceptor differentiation.
Main Methods:
- Gene deletion of Drosophila USP5.
- Analysis of eye development phenotypes.
- Genetic epistasis analysis.
- Molecular marker studies.
Main Results:
- USP5 gene deletion resulted in significant defects in photoreceptor differentiation.
- These developmental defects were primarily caused by the activation of apoptosis.
- The JNK pathway was also found to be activated in usp5 mutants.
Conclusions:
- Drosophila USP5 plays a critical role in regulating apoptosis and JNK pathway signaling during eye development.
- Loss of USP5 function leads to developmental defects through aberrant apoptosis.
- This study provides insights into the conserved function of USP5 homologs, including mammalian USP5.
