Abstract
Plants are constantly exposed to a large and diverse array of microbes; however, most plants are immune to the majority of potential invaders and susceptible to only a small subset of pathogens. The cytoskeleton comprises a dynamic intracellular framework that responds rapidly to biotic stresses and supports numerous fundamental cellular processes including vesicle trafficking, endocytosis and the spatial distribution of organelles and protein complexes. For years, the actin cytoskeleton has been assumed to play a role in plant innate immunity against fungi and oomycetes, based largely on static images and pharmacological studies. To date, however, there is little evidence that the host-cell actin cytoskeleton participates in responses to phytopathogenic bacteria. Here, we quantified the spatiotemporal changes in host-cell cytoskeletal architecture during the immune response to pathogenic and non-pathogenic strains of Pseudomonas syringae pv. tomato DC3000. Two distinct changes to host cytoskeletal arrays were observed that correspond to distinct phases of plant-bacterial interactions i.e. the perception of microbe-associated molecular patterns (MAMPs) during pattern-triggered immunity (PTI) and perturbations by effector proteins during effector-triggered susceptibility (ETS). We demonstrate that an immediate increase in actin filament abundance is a conserved and novel component of PTI. Notably, treatment of leaves with a MAMP peptide mimic was sufficient to elicit a rapid change in actin organization in epidermal cells, and this actin response required the host-cell MAMP receptor kinase complex, including FLS2, BAK1 and BIK1. Finally, we found that actin polymerization is necessary for the increase in actin filament density and that blocking this increase with the actin-disrupting drug latrunculin B leads to enhanced susceptibility of host plants to pathogenic and non-pathogenic bacteria.
Highlights
Actin filament arrays in plant cells undergo constant remodeling and can respond rapidly to a diverse array of extracellular stimuli
We provide the first evidence that the actin cytoskeleton rearranges in response to a phytopathogenic bacterium and we quantified the temporal response of epidermal cells to Pseudomonas syringae pv. tomato DC3000 strains and susceptible Arabidopsis mutants, using a robust set of tools for measuring changes in actin organization
We dissected the initial steps involved in the host-cell signaling pathway and demonstrated that FLAGELLIN-SENSING 2 (FLS2), BAK1, and BIK1 were required for the actin response
Summary
Actin filament arrays in plant cells undergo constant remodeling and can respond rapidly to a diverse array of extracellular stimuli. Cells that are gently prodded with glass or tungsten needles generate extensively bundled filament arrays directly under the site of mechanical stimulation; yet, once the stimulus is removed the bundling is abrogated [5] This is thought to mimic the efforts of fungi and oomycetes to gain entry into plant cells and, as such, it has been commonly assumed that attempted or actual penetration is responsible for eliciting changes in the host-cell actin cytoskeleton, rather than activation of host-cell defense signaling following the recognition of ‘non-self’. For example, initiates a selfincompatibility (SI) response, resulting in massive depolymerization of actin filaments within minutes of stimulus perception, effectively inhibiting pollen tube growth and blocking fertilization [6] In contrast with this signal-mediated destruction of actin filaments, the interaction between mutualistic bacteria and plant cells generally results in the development of bright phalloidindecorated spots in host cells [7] – suggestive of actin polymerization. Nap mutant root hairs, which are incapable of proper nodule formation, lack the ability to elicit
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