Linking Lysosomal Trafficking Defects with Changes in Aging and Stress Response in Drosophila

Anne Simonsen, Robert C. Cumming and Kim D. Finley

volume 3 | issue 5

September/October 2007
Pages: 499 - 501

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Defects in pathways that direct cellular components to the lysosome for degradation are often linked with a decrease in viability and with progressive disorders. Previously we had shown that blue cheese (bchs: Drosophila homologue of human Alfy) mutations lead to reduced longevity and the accumulation of ubiquitinated neural aggregates. A genetic modifier screen based on overexpression of Bchs in the eye was used to identify several potential genetic interactions, which included autophagic and endocytic trafficking genes as well as cytoskeletal and motor proteins and members of the SUMO and ubiquitin signaling pathways. We found that mutations in several of the genes identified in the screen also result in bchs-like phenotypes, including a reduction in adult lifespan and changes in ubiquitinated protein profiles. In addition, we show that Bchs modifiers belonging to the autophagic and trans-Golgi trafficking pathways also display defects in adult starvation response. Our data further support a role for Bchs/Alfy in the autophagic pathway and strongly indicate that autophagy plays an important role in aging and stress response.

Addendum to:
Genetic Modifiers of the Drosophila Blue Cheese Gene Link Defects in Lysosomal Transport with Decreased Lifespan and Altered Ubiquitinated Protein Profiles
A. Simonsen, R. Cumming, K. Lindmo, V. Galaviz, S. Cheng, T. Rusten and K. Finley
Genetics 2007; In press

Authors

Anne Simonsen

The Norwegian Radium Hospital; Oslo, Norway

Robert C. Cumming

The Salk Institute for Biological Studies

Kim D. Finley