Abstract
The discovery of the molecular machinery of autophagy, namely Atg proteins, was awarded with the Nobel prize in physiology and medicine to Yoshinori Ohsumi in 2016. While this machinery was originally identified by its ability to allow cells to survive starvation via lysosomal degradation to recycle cellular components, it has recently become apparent that it also is used by cells to secrete cytoplasmic constituents. Furthermore, viruses have learned to use this Atg supported exocytosis to exit cells, acquire envelopes in the cytosol and select lipids into their surrounding membranes that might allow for increased robustness of their virions and altered infection behavior. Along these lines, picornaviruses exit infected cells in packages wrapped into autophagic membranes, herpesviruses recruit autophagic membranes into their envelopes and para- as well as orthomyxoviruses redirect autophagic membranes to the cell membrane, which increases the robustness of their envelope that they acquire at this site. These recent findings open a new exciting field on the regulation of degradation vs. release of autophagic membranes and will be discussed in this minireview.
Highlights
ON AUTOPHAGYAutophagy or self-eating describes degradation of cytoplasmic constituents in lysosomes, which are able to break down all cellular macromolecules including lipids, polysaccharides, and proteins by virtue of their hydrolases (De Duve and Wattiaux, 1966)
Exosomes released via multivesicular bodies (MVBs) seem to contain lipidated LC3 (Pallet et al, 2013). These studies suggest that autophagosomes can be redirected to MVBs for exocytosis of their inner membrane containing cargo that has been recruited via Atg8 binding. This function obviously differs quite significantly from canonical macroautophagy and it becomes important to define if different substrates are recruited rather to this exocytosis than rather to canonical autophagy, how this is regulated and which machinery diverts these vesicles from lysosomal degradation toward secretion
In addition to acylCoA binding protein 1 (Acb1) and IL-1β, synuclein, amyloid β protein, bone morphogens, and even mitochondria have been suggested to be exocytosed in an Atg dependent fashion (Ejlerskov et al, 2013; Nilsson et al, 2013; Mankelow et al, 2015; Rosenthal et al, 2015), but it needs to be clarified if multiple exocytosis pathways use molecular components of macroautophagy or if only one pathway of autophagic exocytosis exists with many substrates
Summary
Viruses have learned to use this Atg supported exocytosis to exit cells, acquire envelopes in the cytosol and select lipids into their surrounding membranes that might allow for increased robustness of their virions and altered infection behavior. Along these lines, picornaviruses exit infected cells in packages wrapped into autophagic membranes, herpesviruses recruit autophagic membranes into their envelopes and para- as well as orthomyxoviruses redirect autophagic membranes to the cell membrane, which increases the robustness of their envelope that they acquire at this site.
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