%0 Journal Article
%T Selective Autophagy in Drosophila
%A Ioannis P. Nezis
%J International Journal of Cell Biology
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/146767
%X Autophagy is an evolutionarily conserved process of cellular self-eating and is a major pathway for degradation of cytoplasmic material by the lysosomal machinery. Autophagy functions as a cellular response in nutrient starvation, but it is also associated with the removal of protein aggregates and damaged organelles and therefore plays an important role in the quality control of proteins and organelles. Although it was initially believed that autophagy occurs randomly in the cell, during the last years, there is growing evidence that sequestration and degradation of cytoplasmic material by autophagy can be selective. Given the important role of autophagy and selective autophagy in several disease-related processes such as neurodegeneration, infections, and tumorigenesis, it is important to understand the molecular mechanisms of selective autophagy, especially at the organismal level. Drosophila is an excellent genetically modifiable model organism exhibiting high conservation in the autophagic machinery. However, the regulation and mechanisms of selective autophagy in Drosophila have been largely unexplored. In this paper, I will present an overview of the current knowledge about selective autophagy in Drosophila. 1. Introduction Macroautophagy (from hereafter referred to as autophagy) is an evolutionarily conserved process by which a portion of the cytosol and organelles are sequestered by isolation membranes called phagophores. The phagophore engulfs portions of the cytoplasm and forms a double-membrane-layered organelle called the autophagosome. The autophagosome then fuses with a lysosome and generate the autolysosome that has a single limiting membrane, where its sequestered components are degraded [1]. Autophagy serves as a cellular response in nutrient starvation, but it is also responsible for the removal of aggregated proteins, damaged organelles, and developmental remodeling and therefore plays an important role in the quality control of proteins and organelles and in cellular homeostasis [1]. Genetic inhibition of autophagy induces degeneration that resembles degeneration observed during ageing, and physiological ageing is associated with reduced autophagic activity [2]. Autophagy is implicated in neurodegeneration, infections, tumorigenesis, heart disease, liver and lung disease, myopathies, and in lysosomal storage disorders [2]. Interestingly, it has been shown that induction of autophagy can increase longevity in multiple animal species [3]. Contrary to the belief that autophagy is a nonselective process, recent evidence suggests that
%U http://www.hindawi.com/journals/ijcb/2012/146767/