Plant Pathogens Utilize Effectors to Hijack the Host Endoplasmic Reticulum as Part of Their Infection Strategy

摘要

1.Introduction As the central organelle in the eukaryotic secretory pathway,the endoplasmic reticulum(ER)mediates cellular processes that include calcium homeostasis and protein processing[1,2].The infection of plants by pathogens can induce ER stress and trigger the unfolded protein response(UPR).The UPR is a conserved protective signaling pathway that leads to programmed cell death(PCD)under extreme conditions[3–5],which can harm or benefit pathogens,depending on the timing and mode of cell death,and on whether the pathogen has physiologically adapted to benefit from the dying tissue[6].The biosynthesis and proper function of plant pattern recognition receptors(PRRs),which perceive pathogen-or microbe-associated molecular patterns(PAMPs or MAMPs)at the cell surface,also rely on N-glycosylation and the ER quality-control(ERQC)system[7–9].However,pathogens have evolved the capacity utilizing effectors to bind to the host ER stress pathway and manipulate it to their advantage during infection.