Peering into the ‘black box’ of pathogen recognition by cellular autophagy systems

Authors:

Shu-chin Lai# and Rodney J Devenish

doi: 10.15698/mic2015.09.225
Volume 2, pp. 322 to 328, published 22/08/2015.

Affiliations:

Department of Biochemistry and Molecular Biology, Monash University, Clayton campus, Melbourne, Victoria 3800, Australia.

# Current address: Immunobiology and Cancer Research Program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City; Oklahoma 73104, U.S.A.

Keywords: 

autophagy, E3 ligase, galectin-8, tripartite motif proteins, ubiquitin

Corresponding Author(s):

Professor RJ Devenish, rod.devenish@monash.edu

Conflict of interest statement:

The authors declare that they have no competing interests.

Please cite this article as:

Shu-chin Lai and Rodney J Devenish (2015). Peering into the ‘black box’ of pathogen recognition by cellular autophagy systems. Microbial Cell 2(9): 322-328.

© 2015 Lai and Devenish. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

Abstract:

Autophagy is an intracellular process that plays an important role in protecting eukaryotic cells and maintaining intracellular homeostasis. Pathogens, including bacteria and viruses, that enter cells can signal induction of selective autophagy resulting in degradation of the pathogen in the autolysosome. Under such circumstances, the specific recognition and targeting of the invading pathogen becomes a crucial step for the subsequent initiation of selective autophagosome formation. However, the nature of the signal(s) on the pathogen surface and the identity of host molecule(s) that presumably bind the signal molecules remain relatively poorly characterized. In this review we summarise the available evidence regarding the specific recognition of invading pathogens by which they are targeted into host autophagy pathways.