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Tissue-specific autophagy alterations and increased tumorigenesis in mice deficient in Atg4C/autophagin-3

Guillermo Mariño1, Natalia Salvador-Montoliu1, Antonio Fueyo2

  • 1Departamento de Bioquímica y Biología Molecular, Instituto Universitario de Oncología, Universidad de Oviedo, 33006 Oviedo, Spain.

The Journal of Biological Chemistry
|April 20, 2007
PubMed

Insights

Autophagy protein Atg4C is not essential for normal development but is crucial for autophagic activity during starvation. Atg4C deficiency increases susceptibility to chemically induced fibrosarcomas.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Atg4C/autophagin-3 is a cysteine proteinase involved in autophagy.
  • Its precise in vivo function remains unclear.
  • Autophagy is essential for cellular homeostasis and stress response.

Purpose of the Study:

  • To investigate the in vivo role of Atg4C in autophagy.
  • To determine the functional relevance of Atg4C orthologues.
  • To assess the impact of Atg4C deficiency on cellular stress responses and disease.

Main Methods:

  • Generation of Atg4C-deficient mice.
  • Assessment of autophagic activity via immunoblotting and fluorescence microscopy (GFP-LC3 transgenic mice).
  • Evaluation of susceptibility to chemically induced fibrosarcomas.

Main Results:

  • Atg4C-deficient mice are viable and fertile with no obvious abnormalities under normal conditions.
  • Starved Atg4C-deficient mice exhibit decreased autophagic activity in the diaphragm.
  • Atg4C-deficient mice show increased susceptibility to chemically induced fibrosarcomas.

Conclusions:

  • Atg4C is not essential for basal autophagy but is required for efficient autophagic response under stress (e.g., starvation).
  • Atg4C may play a role in tumor progression in vivo.
  • Further research is needed to elucidate the precise mechanisms of Atg4C in autophagy and cancer.

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