Research into the interplay between plants and bacteria could lead to new chemical-free pathways of protecting plants
The intimate interaction between a plant and its environment has sent some puzzling cues to scientists trying to determine how, at the molecular level, a plant becomes infected by bacteria. At this level, researchers have found that plants sometimes beckon the bacteria in a seemingly counterintuitive action to its health.
A team of researchers, led by Scott Peck at the University of Missouri’s Bond Life Sciences Center, discovered how a plant’s own chemicals act as a beacon to bacteria triggering an infection. The work, which Peck calls “a very nice example of why basic science is important,” could lead to “a completely new mechanism for improving bacterial resistance.”
Peck’s team worked with a mutant mustard plant called Arabidopsis mkp1, which appeared to be resistant to bacterial infection. Discovered several years ago by Peck’s lab, this little mustard plant acts differently than others by rebuffing the advances of bacteria. Lab tests confirmed that Arabidopsis mkp1 didn’t get infected by Pseudomonas syringae pv. tomato DC3000, a bacterial pathogen that causes brown spots on tomatoes and hurts the model plant Arabidopsis.
In normal conditions, once bacteria recognizes host-plant chemicals “it builds a needle-like syringe that injects 20 to 30 proteins into the host shutting down the plant’s immune system,” said Peck, a plant scientist who has studied plant-microbe interactions for the past 16 years. “Without a proper defense response, bacteria will grow and continue to infect the plant.”
Peck’s group found that in order to detect a host plant, bacteria need to sense a sugar, which plants produce abundantly through photosynthesis, and at least one of five acids (aspartic, citric, pyroglutamic, 4-hydrobenzoic and shikimic) at the same time. Once a host is detected, the bacteria deploy a Type III secretion system (the needle-like syringe and associated proteins). But in the case of Arabidopsis mkp1, the mutant plant did not trigger the bacteria’s Type III secretion system.
In addition, Peck said, the mutant’s resistance “did not seem to fit with the pathways normally associated with resistance in plants. We knew mkp1 was showing us something unique, but we just didn’t know what it was.”
A research team at Pacific Northwest National Laboratory worked with Peck’s group to compare levels of metabolites between the mutant Arabidopsis and normal plants. This comparison helped Peck identify a few of these chemicals – created from regular plant processes – that existed in much lower levels in the mutant.
Using the PNNL work as a guide, the Missouri team identified the five acids that seemed to have the biggest effect in turning on a bacterial infection.
“The key experiment involved us simply adding these acids back into the mutant,” Peck said. “Suddenly we saw the mutant plant wasn’t resistant anymore and the bacteria were once again capable of injecting proteins to turn off the plant’s immune system.”
Further studies showed that while low concentrations of at least one of these five acids trigger the bacteria’s attack, high levels blind it to the plant’s presence, leading Peck to believe the discovery could be used to hinder bacterial growth.
He added that “there is sort of a three-tier system” at work. In the mkp1 mutant the acids are present but too low to induce the bacteria, in normal plants there are ”low” physiological levels that induce the bacteria, and their experiments showed high (five times and greater than physiological) concentrations can suppress infection.
Peck added that if this discovery can be used to actually thwart the bacteria’s head start on the plant’s immune system, it could mean stopping disease in crops and lead to a different approach in the field.
“Our work is the first to clearly demonstrate using genetics what these signals are and that regulation of these host signals can alter the outcome of host-pathogen interactions,” Peck explained. “If we can make the potential pathogen ‘blind’ to the signals it needs to become infectious, it may be possible to produce resistant plants without having to try to kill the bacteria.
“This could be done genetically as we have done with Arabidopsis. Or, now that we have defined the host signals, we may be able to use this knowledge to target the bacterial perception system(s). This strategy could ultimately lead to a new generation of bacteriostatic antimicrobials,” he added.
Peck and his University of Missouri colleagues – Jeffrey Anderson and Ying Wan – reported their findings in the April 21 issue of the Proceedings of the National Academy of Sciences.