Impaired G1-Arrest, Autophagy, and Apoptosis in Atg7-Knockout Mice
Atg7 Modulates p53 Activity to Regulate Cell Cycle and
Survival During Metabolic Stress
Lee et al
Exit from cell division cycle, induction of autophagy, and activation of apoptosis in response to metabolic stress occur simultaneously or sequentially. However, the molecular interrelation(s) between these intracellular events remains obscure. Recent work by Finkel et al1 provides evidence that Atg7, an autophagy-related protein, regulates G1-arrest by interacting with p53 and that p53-mediated apoptosis is activated under autophagy-deficient conditions.
Macroautophagy (hereafter referred to as autophagy) is a self-eating system conserved among eukaryotes. In this process, cellular components, including organelles, are entrapped into a double-membrane structure called the autophagosome and then degraded by lysosomal hydrolases (Figure 1).2 In addition to its role in supplying amino acids in response to nutrient starvation, autophagy is involved in quality control to maintain cell health. Thus, inactivation of autophagy results in the accumulation of cytoplasmic protein aggregates of misfolded proteins and damaged and degenerated organelles, which compromise cell function and often result in life-threatening diseases.2