Autophagy is an evolutionarily conserved intracellular degradation process, through which large cellular cargos are sequestered into double-membrane vesicles (autophagosomes) and delivered to the lysosome. Starvation-induced autophagy represents a general non-selective degradation pathway that breaks down cellular components for energy replenishment. Alternatively, selective autophagy targets specific organelles, protein aggregates or invading pathogens that need to be precisely removed from the cell during development or pathogenic infection. Selective autophagy receptors noncovalently bind to the family of ATG8 modifiers and can be controlled by post-translational protein modifications, including ubiquitination and phosphorylation. In this article, we review recent advances in our understanding of the molecular basis of cargo selection in autophagy.

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