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Atg7 Modulates p53 Activity to Regulate Cell Cycle and Survival During Metabolic Stress

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Science  13 Apr 2012:
Vol. 336, Issue 6078, pp. 225-228
DOI: 10.1126/science.1218395

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Starvation and Autophagy

Starvation stimulates withdrawal from the cell cycle, as well as stimulating autophagy. Are these two events connected? Lee et al. (p. 225) show a direct and nutrient-sensitive interaction between the tumor suppressor p53 and the essential autophagy gene Atg7. Further, in the absence of Atg7, the p53-dependent induction of the cyclin-dependent kinase inhibitor p21 is inhibited. This leads to Atg7-deficient cells being unable to properly withdraw from the cell cycle under starved conditions. While Atg7 deletion leads to an impairment of p53-mediated cell-cycle arrest, the Atg7-deficient cells hyperactivate p53-mediated cell-death pathways. The physiological importance of this hyperactivation is underscored by the observation that genetic blocking of p53-mediated cell death significantly extended neonatal survival of mice in which Atg7 had been deleted.

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