Rerouting of selective autophagy towards the haustorial interface by Phytophthora infestans
Y. DAGDAS (1), K. Belhaj (1), A. Maqbool (2), A. Chaparro-Garcia (1), P. Pandey (3), N. Cruz-Mireles (1), B. Petre (1), N. Tabasum (3), R. Hughes (2), J. Sklenar (1), J. Win (1), F. Menke (1), K. Findlay (4), M. Banfield (2), T. Bozkurt (3), S. Kamoun (1) (1) The Sainsbury Laboratory, United Kingdom; (2) John Innes Centre, Department of Biological Chemistry, United Kingdom; (3) Imperial College, London, United Kingdom; (4) John Innes Centre, Department of Cell and Developmental Biology, United Kingdom

Autophagy is a multifaceted membrane trafficking pathway essential for cellular homeostasis. It is driven by autophagosomes, double-membrane vesicles decorated with conserved ubiquitin-like proteins called ATG8. It is now well established that rather than being a bulk degradation process, autophagy is highly selective. Autophagy receptors bind ATG8 and mediate selective transport of autophagosomes to various compartments. These receptors interact with ATG8 via a conserved ATG8 Interacting Motif (AIM). The mechanisms by which autophagy contributes to immunity remain poorly understood. Also, the degree to which plant pathogens have evolved to target and interfere with autophagy related processes is unknown. Recently, we showed that PexRD54, an effector from 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. Then, we investigated subcellular dynamics of selective autophagy in haustoriated cells. PexRD54 subverts selective autophagy to divert ATG8CL autophagosomes to the haustorial interface possibly to reattribute cellular resources. It also prevents haustorial accumulation of Joka2 labeled autophagosomes that contain defense related cargoes. Thus the pathogen coopts the host cell’s endomembrane compartment to promote its own growth at the cost of the cell’s physiology.

Abstract Number: P7-164
Session Type: Poster