Host autophagy machinery is diverted to the pathogen interface to
mediate focal defense responses against the Irish potato famine
pathogen
mediate focal defense responses against the Irish potato famine
pathogen
File(s)
Published version
OA Location
Author(s)
Type
Journal Article
Abstract
During plant cell invasion, the oomycete Phytophthora infestans remains enveloped by
host-derived membranes whose functional properties are poorly understood. P. infestans secretes
a myriad of effector proteins through these interfaces for plant colonization. Recently we showed
that the effector protein PexRD54 reprograms host-selective autophagy by antagonising
antimicrobial-autophagy receptor Joka2/NBR1 for ATG8CL binding (Dagdas et al., 2016). Here, we
show that during infection, ATG8CL/Joka2 labelled defense-related autophagosomes are diverted
toward the perimicrobial host membrane to restrict pathogen growth. PexRD54 also localizes to
autophagosomes across the perimicrobial membrane, consistent with the view that the pathogen
remodels host-microbe interface by co-opting the host autophagy machinery. Furthermore, we
show that the host-pathogen interface is a hotspot for autophagosome biogenesis. Notably,
overexpression of the early autophagosome biogenesis protein ATG9 enhances plant immunity.
Our results implicate selective autophagy in polarized immune responses of plants and point to
more complex functions for autophagy than the widely known degradative roles.
host-derived membranes whose functional properties are poorly understood. P. infestans secretes
a myriad of effector proteins through these interfaces for plant colonization. Recently we showed
that the effector protein PexRD54 reprograms host-selective autophagy by antagonising
antimicrobial-autophagy receptor Joka2/NBR1 for ATG8CL binding (Dagdas et al., 2016). Here, we
show that during infection, ATG8CL/Joka2 labelled defense-related autophagosomes are diverted
toward the perimicrobial host membrane to restrict pathogen growth. PexRD54 also localizes to
autophagosomes across the perimicrobial membrane, consistent with the view that the pathogen
remodels host-microbe interface by co-opting the host autophagy machinery. Furthermore, we
show that the host-pathogen interface is a hotspot for autophagosome biogenesis. Notably,
overexpression of the early autophagosome biogenesis protein ATG9 enhances plant immunity.
Our results implicate selective autophagy in polarized immune responses of plants and point to
more complex functions for autophagy than the widely known degradative roles.
Date Issued
2018-06-22
Date Acceptance
2018-06-22
Citation
eLife, 2018, 7
ISSN
2050-084X
Publisher
eLife Sciences Publications Ltd
Journal / Book Title
eLife
Volume
7
Copyright Statement
Copyright © Dagdas et al. This
article is distributed under the
terms of the Creative Commons
Attribution License, which
permits unrestricted use and
redistribution provided that the
original author and source are
credited.
article is distributed under the
terms of the Creative Commons
Attribution License, which
permits unrestricted use and
redistribution provided that the
original author and source are
credited.
Sponsor
Biotechnology and Biological Sciences Research Council (BBSRC)
Biotechnology and Biological Sciences Research Council (BBSRC)
Biotechnology and Biological Sciences Research Council (BBSRC)
Grant Number
BB/M002462/1
4020014827
BB/GCRF-IAA/17/10
Subjects
Science & Technology
Life Sciences & Biomedicine
Biology
Life Sciences & Biomedicine - Other Topics
PHYTOPHTHORA-INFESTANS
CELL BIOLOGY
ENDOCYTIC TRAFFICKING
SUBCELLULAR RESPONSES
APOPLASTIC EFFECTORS
SELECTIVE AUTOPHAGY
PLANT-PATHOGENS
PROTEIN
ARABIDOPSIS
INFECTIONS
RXLR Effector
autophagosome
cell biology
defense-related autophagy
effector biology
haustoria
nicotiana benthamiana
phytophthora infestans
plant biology
plant immunity
selective autophagy
Publication Status
Published
Article Number
e37476