Abstract
A hallmark of multicellular organisms is their ability to maintain physiological homeostasis by communicating among cells, tissues, and organs. In plants, intercellular communication is largely dependent on plasmodesmata (PD), which are membrane-lined channels connecting adjacent plant cells. Upon immune stimulation, plants close PD as part of their immune responses. Here, we show that the bacterial pathogen Pseudomonas syringae deploys an effector protein, HopO1-1, that modulates PD function. HopO1-1 is required for P. syringae to spread locally to neighboring tissues during infection. Expression of HopO1-1 in Arabidopsis (Arabidopsis thaliana) increases the distance of PD-dependent molecular flux between neighboring plant cells. Being a putative ribosyltransferase, the catalytic activity of HopO1-1 is required for regulation of PD. HopO1-1 physically interacts with and destabilizes the plant PD-located protein PDLP7 and possibly PDLP5. Both PDLPs are involved in bacterial immunity. Our findings reveal that a pathogenic bacterium utilizes an effector to manipulate PD-mediated host intercellular communication for maximizing the spread of bacterial infection.
Highlights
Multicellular organisms host a wide array of microorganisms
Bacterial effectors have been detected in different cellular compartments within plant cells, including the plasma membrane (PM) (Shan et al, 2000; Robert-Seilaniantz et al, 2006; Xin et al, 2015), endoplasmic reticulum (Block et al, 2014), trans-Golgi network (TGN)/early endosome (EE) (Nomura et al, 2011), chloroplast (Jelenska et al, 2007; Li et al, 2014), mitochondrion (Block et al, 2009), and nucleocytoplasm (Fu et al, 2007; Giska et al, 2013)
We found no evidence that PDLP1 is involved in Pst DC3000 infection of Arabidopsis
Summary
Multicellular organisms host a wide array of microorganisms. most microbes are beneficial or harmless to their hosts, infections caused by a few pathogenic microorganisms can lead to devastating diseases in animals and plants. Plants detect the presence of microorganisms by recognizing microbial signatures such as bacterial flagellin and fungal chitin, collectively known as microbe-associated molecular patterns (MAMPs; Ranf, 2017). Recognition of MAMPs by membrane-bound pattern recognition receptors (PRRs) on the plant cell surface initiates a cascade of signaling events, activating a form of plant innate immunity known as pattern-triggered immunity (PTI; Ranf, 2017; Saijo et al, 2018). Pathogenic microbes deliver virulence-intended microbial molecules, collectively called “effectors”, mostly into host cells as a major pathogenesis mechanism (Grant et al, 2006; Le Fevre et al, 2015; Toruno et al, 2016). Current models suggest that pattern-triggered immunity and effector-triggered immunity constitute two major forms of cellautonomous immunity in plants
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