An effector of the Irish potato famine pathogen antagonizes a host autophagy cargo receptor
- The Sainsbury Laboratory, United Kingdom
- John Innes Centre, United Kingdom
- Imperial College London, United Kingdom
Abstract
Plants use autophagy to safeguard against infectious diseases. However, how plant pathogens interfere with autophagy related processes is unknown. Here we show that PexRD54, an effector from the Irish potato famine pathogen Phytophthora infestans, binds host autophagy protein ATG8CL to stimulate autophagosome formation. PexRD54 depletes the autophagy cargo receptor Joka2 out of ATG8CL complexes and interferes with Joka2's positive effect on pathogen defense. Thus a plant pathogen effector has evolved to antagonize a host autophagy cargo receptor in order to counteract host defenses.
Article and author information
Author details
Reviewing Editor
- Jean T Greenberg, University of Chicago, United States
Version history
- Received: August 15, 2015
- Accepted: January 13, 2016
- Accepted Manuscript published: January 14, 2016 (version 1)
- Version of Record published: February 23, 2016 (version 2)
- Version of Record updated: October 6, 2016 (version 3)
Copyright
© 2016, Dagdas et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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An effector of the Irish potato famine pathogen antagonizes a host autophagy cargo receptor
eLife 5:e10856.
https://doi.org/10.7554/eLife.10856
Further reading
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- Microbiology and Infectious Disease
- Plant Biology
Pathogens target proteins involved in autophagy to inhibit immune responses in plants.
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- Microbiology and Infectious Disease
Antimicrobial resistance (AMR) poses a significant threat to human health. Although vaccines have been developed to combat AMR, it has proven challenging to associate specific vaccine antigens with AMR. Bacterial plasmids play a crucial role in the transmission of AMR. Our recent research has identified a group of bacterial plasmids (specifically, IncHI plasmids) that encode large molecular mass proteins containing bacterial immunoglobulin-like domains. These proteins are found on the external surface of the bacterial cells, such as in the flagella or conjugative pili. In this study, we show that these proteins are antigenic and can protect mice from infection caused by an AMR Salmonella strain harboring one of these plasmids. Furthermore, we successfully generated nanobodies targeting these proteins, that were shown to interfere with the conjugative transfer of IncHI plasmids. Considering that these proteins are also encoded in other groups of plasmids, such as IncA/C and IncP2, targeting them could be a valuable strategy in combating AMR infections caused by bacteria harboring different groups of AMR plasmids. Since the selected antigens are directly linked to AMR itself, the protective effect extends beyond specific microorganisms to include all those carrying the corresponding resistance plasmids.
