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Atg7 modulates p53 activity to regulate cell cycle and survival during metabolic stress

In Hye Lee1, Yoshichika Kawai, Maria M Fergusson

  • 1Center for Molecular Medicine, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA.

Science (New York, N.Y.)
|April 14, 2012
PubMed

Insights

Autophagy gene Atg7 is crucial for cell cycle arrest during nutrient withdrawal. It regulates p53, controlling cell division and apoptosis, preventing DNA damage and lethality in mice.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Nutrient withdrawal triggers cell cycle arrest, autophagy, and cell death.
  • The interplay between these stress responses is not fully understood.

Purpose of the Study:

  • To investigate the role of autophagy gene Atg7 in cellular responses to nutrient deprivation.
  • To elucidate the relationship between Atg7, cell cycle regulation, and cell death pathways.

Main Methods:

  • Utilized mouse embryonic fibroblasts lacking Atg7.
  • Analyzed cell cycle progression, p53 binding, p21(CDKN1A) transcription, DNA damage, and apoptosis.
  • Investigated the effect of Chk2 deletion on Atg7(-/-) mouse survival.

Main Results:

  • Atg7-deficient cells failed to arrest the cell cycle upon starvation.
  • Atg7 directly bound to p53, regulating p21(CDKN1A) expression independently of its enzymatic activity.
  • Absence of Atg7 led to increased DNA damage and p53-dependent apoptosis under prolonged stress.
  • Inhibiting the DNA damage response partially rescued lethality in Atg7(-/-) mice.

Conclusions:

  • Atg7 is essential for nutrient-deprivation-induced cell cycle arrest.
  • Atg7 modulates p53 activity to control cell cycle arrest and apoptosis.
  • Atg7 plays a critical role in managing cellular stress responses to nutrient limitation.

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