Drosophila USP5 controls the activation of apoptosis and the Jun N-terminal kinase pathway during eye development

PLoS One. 2014 Mar 18;9(3):e92250. doi: 10.1371/journal.pone.0092250. eCollection 2014.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Cell Differentiation
  • Compound Eye, Arthropod / cytology
  • Compound Eye, Arthropod / enzymology*
  • Compound Eye, Arthropod / growth & development
  • Drosophila Proteins / physiology*
  • Drosophila melanogaster / cytology
  • Drosophila melanogaster / enzymology*
  • Drosophila melanogaster / growth & development
  • Gene Knockout Techniques
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • MAP Kinase Signaling System*
  • Photoreceptor Cells, Invertebrate / physiology
  • Polyubiquitin / metabolism
  • Ubiquitin-Specific Proteases / physiology*
  • Ubiquitination

Substances

  • Drosophila Proteins
  • Polyubiquitin
  • JNK Mitogen-Activated Protein Kinases
  • USP5 protein, Drosophila
  • Ubiquitin-Specific Proteases

Grants and funding

This work was supported by grants from the National Basic Research Program of China (No. 2011CB943900). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.