Atg7-dependent autophagy promotes neuronal health, stress tolerance, and longevity but is dispensable for metamorphosis in Drosophila

Gábor Juhász, Balázs Érdi, Miklós Sass, Thomas P. Neufeld

Research output: Contribution to journalArticlepeer-review

277 Scopus citations

Abstract

Autophagy, a cellular process of cytoplasmic degradation and recycling, is induced in Drosophila larval tissues during metamorphosis, potentially contributing to their destruction or reorganization. Unexpectedly, we find that flies lacking the core autophagy regulator Atg7 are viable, despite severe defects in autophagy. Although metamorphic cell death is perturbed in Atg7 mutants, the larval-adult midgut transition proceeds normally, with extended pupal development compensating for reduced autophagy. Atg7?/? adults are short-lived, hypersensitive to nutrient and oxidative stress, and accumulate ubiquitin-positive aggregates in degenerating neurons. Thus, normal levels of autophagy are crucial for stress survival and continuous cellular renewal, but not metamorphosis.

Original languageEnglish (US)
Pages (from-to)3061-3066
Number of pages6
JournalGenes and Development
Volume21
Issue number23
DOIs
StatePublished - Dec 1 2007

Keywords

  • Atg7
  • Autophagy
  • Drosophila
  • Longevity
  • Metamorphosis
  • Neurodegeneration

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