Dr. Alan Collmer studies plant-pathogen warfare. On Thursday, Oct 20th, he spoke to the PSLA department about the infection strategies of Pseudomonas syringae, a pathogen whose complete genome he helped to sequence (Buell et al., 2003).
To infect plant tissues, pathogens use weapons, called effectors. P. syringae DC3000 injects 30 effectors into plant cells by the type III secretion system (T3SS). However, of these 30, only 8 are required to fully damage the plant, and the rest are redundant, meaning they can be held in reserve and deployed as plant defenses shift. Type III effectors (T3Es) are like assassins because they silence a plant defense called pattern-triggered immunity (PTI), while eluding internal surveillance by plant resistance (R) proteins that trigger effector-triggered immunity (ETI) (Collmer, 2016).
Dr. Collmer wanted to know about T3E interactions, how they evolve to match ever-adapting plant defenses, and the role of redundancy in this plant-pathogen arms race. To study the roles of specific effectors, Dr. Collmer’s lab deleted 28 T3E genes to produce a mutant called DC3000D28E. They then restored an effector gene called avrPtoB and 7 other T3E genes. Although this mutant seemed effectorless, it killed plant cells when injected at high inoculum levels. Its ability to block the plant from producing reactive oxygen species (ROS) was surprising because all highly expressed T3E genes had been deleted. These findings revealed that an effector (called HopAD1) was responsible for cell death and ROS suppression. Further study showed that HopAD1 is an avirulence determinant, meaning it decides whether the invasion succeeds. AvrPtoB blocks HopAD1 from killing plant cells and over evolutionary time has developed several virulence activities that hamper each other but make it possible for P. syringae to adapt to many hosts (Wei et al., 2015).
In search of the cell death factor produced in DC300028E, Dr. Collmer’s lab knocked out 36 effectors, creating another mutant called DC3000D36E. Again, a few effector genes were restored to the mutant, including AvrPtoB. Unexpectedly, either hopQ1-1 or hopAD1 can act alone to trigger ETI in DC3000D29E or DC300028E but both must be present to trigger ETI in Pst DC3000. These results indicate that an AvrPtoB activity interacts with an ancient immune signaling component to suppress ETI triggered by HopAD1 and other T3E’s, giving the pathogen virulence (Wei et al., 2015).
This research is essential for deepening our understanding of plant-pathogen interactions, and is a stepping-stone that may lead to the development of new crop disease controls.
Collmer, Alan. “Pseudomonas syringae-plant interactions: Learning the rules of the game by playing with fewer pieces.” University of Maryland at College Park. 20 October 2016. Plant Science Lecture Series.
(“EduOutreach-CastleAttack @ www.pseudomonas-syringae.org,” cartoon by Magdalen Lindeberg)
Buell, C.R., Joardar, V., Lindeberg, M., Selengut, J., Paulsen, I.T., Gwinn, … Collmer, A. (2003). The complete sequence of the Arabidopsis and tomato pathogen Pseudomonas syringae pv. tomato DC3000. Proc. Natl. Acad. Sci. USA 100, 10181-10186.
https://doi.org/10.1073/pnas.1731982100
Wei, H. L., Chakravarthy, S., Mathieu, J., Helmann, T. C., Stodghill, P., Swingle, B., … Collmer, A. (2015). Pseudomonas syringae pv. tomato DC3000 Type III Secretion Effector Polymutants Reveal an Interplay between HopAD1 and AvrPtoB. Cell Host and Microbe, 17(6), 752–762. https://doi.org/10.1016/j.chom.2015.05.007
