Abstract
The eukaryotic cytoskeleton is essential for structural support and intracellular transport, and is therefore a common target of animal pathogens. However, no phytopathogenic effector has yet been demonstrated to specifically target the plant cytoskeleton. Here we show that the Pseudomonas syringae type III secreted effector HopZ1a interacts with tubulin and polymerized microtubules. We demonstrate that HopZ1a is an acetyltransferase activated by the eukaryotic co-factor phytic acid. Activated HopZ1a acetylates itself and tubulin. The conserved autoacetylation site of the YopJ / HopZ superfamily, K289, plays a critical role in both the avirulence and virulence function of HopZ1a. Furthermore, HopZ1a requires its acetyltransferase activity to cause a dramatic decrease in Arabidopsis thaliana microtubule networks, disrupt the plant secretory pathway and suppress cell wall-mediated defense. Together, this study supports the hypothesis that HopZ1a promotes virulence through cytoskeletal and secretory disruption.
Highlights
The disruption of critical host cellular structures and processes is an important virulence tactic employed by bacterial pathogens of both plants and animals [1,2]
We show that HopZ1a, from the phytopathogen Pseudomonas syringae is an acetyltransferase that binds plant tubulin
In plants, activated HopZ1a causes a dramatic destruction of microtubule networks, inhibits protein secretion, and suppresses cell wall-mediated defense
Summary
The disruption of critical host cellular structures and processes is an important virulence tactic employed by bacterial pathogens of both plants and animals [1,2]. Many Gram-negative bacterial pathogens accomplish this goal using the type III secretion system (T3SS) to inject virulence proteins known as type III secreted effectors (T3SEs) directly into the host cytosol [3]. One of the major virulence functions of phytopathogen T3SEs is to block host immune responses [4,5]. These T3SEs employ a range of biochemical activities to modify host cell proteins and promote the infection process [6,7]. T3SEs from phytopathogenic bacteria can act as either virulence or avirulence factors that promote bacterial growth or induce host immunity, respectively
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