This study investigates the role of autophagy in mice using conditional knockout mice of Atg7, a gene essential for autophagy in yeast. Atg7 deficiency leads to impaired autophagosome formation and starvation-induced degradation of proteins and organelles. Mice homozygous for the Atg7 knockout allele (Atg7−/−) die within 1 day after birth, while heterozygous mice (Atg7+/−) survive but have reduced body weight and lower amino acid levels. Autophagosome formation is severely impaired in the liver of Atg7-deficient mice under fasting conditions, and the degradation of proteins and organelles is largely impaired. Atg7 deficiency also results in hepatomegaly, accumulation of abnormal organelles, and the formation of ubiquitin-positive aggregates. These findings highlight the importance of autophagy in nutrient recycling, cellular remodeling, and quality control of proteins and organelles in quiescent cells.This study investigates the role of autophagy in mice using conditional knockout mice of Atg7, a gene essential for autophagy in yeast. Atg7 deficiency leads to impaired autophagosome formation and starvation-induced degradation of proteins and organelles. Mice homozygous for the Atg7 knockout allele (Atg7−/−) die within 1 day after birth, while heterozygous mice (Atg7+/−) survive but have reduced body weight and lower amino acid levels. Autophagosome formation is severely impaired in the liver of Atg7-deficient mice under fasting conditions, and the degradation of proteins and organelles is largely impaired. Atg7 deficiency also results in hepatomegaly, accumulation of abnormal organelles, and the formation of ubiquitin-positive aggregates. These findings highlight the importance of autophagy in nutrient recycling, cellular remodeling, and quality control of proteins and organelles in quiescent cells.