Manipulation of the Host Endomembrane System by Bacterial Effectors

Abstract

The endomembrane system, extending from the nuclear envelope to the plasma membrane, is critical to the plant response to pathogen infection. Synthesis and transport of immunity-related proteins and antimicrobial compounds to and from the plasma membrane are supported by conventional and unconventional processes of secretion and internalization of vesicles, guided by the cytoskeleton networks. Although plant bacterial pathogens reside mostly in the apoplast, major structural and functional modifications of the endomembrane system in the host cell occur during bacterial infection. Here, we review the dynamics of these cellular compartments, briefly for their essential contributions to the plant defense responses and in parallel, for their emerging roles in bacterial pathogenicity. We further focus on Pseudomonas syringae, Xanthomonas spp. and Ralstonia solanacearum type III secreted effectors that localize to and/or associate with components of the host endomembrane system or the cytoskeleton network to highlight the diversity of virulence strategies deployed by bacterial pathogens beyond the inhibition of the secretory pathway.

The Pseudomonas syringae pv. tomato DC3000 effector HopD1 interferes with cellular dynamics associated with the function of the plant immune protein AtNHR2B

“…The co-localization of HopD1-GFP with AtNHR2B-RFP was found to be in cytoplasm and in small subcellular compartments (vesicles) of the endomembrane system where AtNHR2B was previously found to be localized (Singh et al, 2018). The localization of AtNHR2B to compartments of the endomembrane systems suggests a function in vesicle trafficking which mediates cellular processes such as endocytosis and secretion (Jeon and Segonzac, 2023). During plant immunity, endocytosis mediates the internalization of PAMPs-activated PRR which in turn induces downstream signaling pathways involved in plant defense (Robatzek Chinchilla et al, 2007;Ben Khaled et al, 2015;Mbengue et al, 2016;Gu et al, 2017).Vesicle trafficking events also mediate secretory processes, which in the context of plant immunity are responsible for the remodeling of the cell wall, the release of antimicrobials to the apoplast and the replenishing of PRR to the plasma membrane (Kwon et al, 2008;Kim and Brandizzi, 2014).…”

XopM, a FFAT motif containing type-III effector protein fromXanthomonas, suppresses PTI responses at the plant plasma membrane

“…Plant bacterial pathogens mostly multiply within the apoplastic space of the infected tissue and therefore an effective defense response is heavily dependent on the extracellular release of defense-related molecules, such as pathogenesis-related proteins, secondary metabolites and cell wall materials. Thus, it does not come as a surprise that secretory and endocytic membrane trafficking pathways lie at the heart of plant’s immune system (Jeon & Segonzac, 2023, Gu et al ., 2017, Yun & Kwon, 2017).…”

“…The injection of type III effector (T3E) proteins into the host cell is an efficient mechanism employed by many Gram-negative bacterial pathogens to overcome MTI and establish a favorable environment (Büttner, 2016, Khan et al ., 2018, Macho & Zipfel, 2015). T3Es encode proteins with diverse biochemical activities which interfere with host cellular processes on all levels of the plants immune response, including ER – mediated processes or vesicle trafficking (Jeon & Segonzac, 2023, Yun et al ., 2023).…”

Logistics of defense: The contribution of endomembranes to plant innate immunity

“…Coevolution of plant–pathogen interactions has led plants to adopt multiple defense strategies exhibiting functional diversification and partial redundancy ( Upson et al, 2018 ; Derevnina et al, 2021 ). In turn, pathogens have evolved effectors aimed at avoiding detection, subverting immune pathways, and maintaining a virulent advantage ( Yuen et al, 2023 ; Jeon and Segonzac, 2023 ). We will take an inside-out view of a cell under pathogen attack, starting from the ER and ending in the extracellular space, and we will discuss how preformed organelles and mechanisms of defense are targeted by pathogens to dampen immunity, and how plants respond to this challenge.…”