WOULD YOU believe that a pathogen infecting plants can force its host to produce nutrients for it? It is odd indeed but true. A species of bacteria that infect corn crops compel their hosts to produce a bunch of nutrients that keeps the pathogens alive and thriving long before they start to kill the plant’s cells. The bacterial pathogen is Pantoea stewartii that infects corn causing Stewarts’ wilt disease.

The study in young maize plants reveals that these bacteria not only generate food for themselves in crops they inhabit, but also coax life-sustaining water from the plants. A bacterial virulence factor, a protein called WtsE, initiates the mobilization of food and water into spaces where the bacteria reside.

No one has shown before that a dynamic flow of nutrients from plant to bacteria supports proliferation of the bacteria during the initial stages of infection.

There have been no targeted efforts to control nutrient availability as a means to control Pantoea stewartii, or other plant pathogenic bacteria that rely on proteins similar to WtsE for their virulence.

The research focuses on a phase called biotrophy: After infecting a plant, the bacteria initially parasitize living host cells and multiply dramatically. Only later do the bacteria start killing plant cells to release further nutrients and cause disease.

For this study, researchers infiltrated maize seedlings with a powerful dose of the infectious bacteria, creating a series of uniformly infected leaves. This model system made it possible for the researchers to determine that the release of nutrients and water preceded the death of plant cells.

The team zeroed in on observing the actions of WtsE, one of a class of proteins in pathogenic bacteria known as type III effectors. These proteins are transported from the bacteria into infected plant cells to both suppress plant immunity and, as discovered in the case of Pantoea stewartii, promote availability of water and food.

All of this activity takes place in the apoplast, a relatively dry compartment on the interior of a plant tissue but outside of the plant cells. That dryness is relevant, because one of WtsE’s tricks is promoting the availability of water in this space. A leading hypothesis has been that this condition, called “water soaking,” results from dying plant cells spilling their contents into the apoplast when bacteria begin their lethal attack.

And then, once hydrated, the apoplast begins to fill with nutrients that function as sources of nitrogen and carbon for the bacteria – sugars, amino acids and organic acids that are generated and consumed in much higher quantities than existing in the apoplast of a healthy plant.

The plant metabolic networks respond to the depletion by making more of those compounds. It’s a really dynamic process and the WtsE effector drives that process. The role of the effector was confirmed genetically – mutant bacteria lacking WtsE were unable to accomplish these same tasks. With these findings, it is now possible to pinpoint how WtsE is able to coerce maize into doing its bidding – and specifically, which plant proteins the effector hijacks for help – which could inform future resistant breeding practices. By Manny Palomar, PhD (EV Mail December 19-25, 2022 issue)