Bacteria force plants to produce a feast of nutrients that support pathogens before they kill corn cells
Corn crops face a variety of bacterial threats but one species of bacteria, Pantoea stewartii, which causes Stewart’s wilt, takes that threat further than most.
In a gorging frenzy, they feed themselves by forcing the plant to produce a feast of nutrients that keep the pathogens alive before they kill the corn cells.
In addition, the bacteria promote a condition called water soaking, which provides life-sustaining water for their own benefit.
The fundamental biological processes behind this destructive gobbling obsession were discovered by researchers at Ohio State University.
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“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,” said David Mackey, professor of horticulture and crop science and a professor of molecular genetics.
“Our early observations that the bacteria cause water-soaking and reprogram metabolism inside the plant cells led us to hypothesize that the reprogramming was intended (at least in part) to facilitate nutrient availability for the bacteria. A significant aspect is that those nutrients become available during biotrophy when the parasite feeds on living plant cells that are still intact. P. stewartii are nasty, thieving little bacteria.”
The bacteria are carried to the plant by corn flea beetles, where they are deposited in wound sites made by the beetles when feeding on crop stems and leaves.
In the study of young plants, Mackey and his team infected corn seedlings with a strong dose of bacteria. The infected leaves allowed the researchers to follow what the bacteria did and confirm that the plants’ release of nutrients and water preceded the death of their cells.
This was the result of the actions of WtsE, one of a class of proteins in pathogenic bacteria known as type lll effectors. They modulate cellular pathways for the benefit of a pathogens and promote bacterial growth. The proteins move from the bacteria into the infected parts of the plant cells to suppress plant immunity and drive the availability of food and water.
The activity takes place in the apoplast, a relative dry compartment inside the plant tissue but outside the plant cells. The bacteria park themselves in the apoplast for a reason because as WtsE promotes water it accumulates in this space.
According to a news release on the research, a leading hypothesis has been that this water soaking results from the plant cells spilling their contents into the apoplast.
“This is one of the main points we showed that infection causes water to accumulate in the apoplast well in advance of killing the plant cells,” said Mackey. “It’s an active process and it’s dependent on the WtsE effector.”
He said that the WtsE protein is part of a broader AvrE-family of effectors distributed across numerous genera of plant-pathogenic bacteria.
“The genes encoding the AvrE-family proteins are part of the collection of genes that encode for the type III secretion apparatus. We assume that the overall function of the AvrE-family effectors is common (e.g., promoting water and nutrient availability). However, individual family members and their pathogens (bacteria) have certainly co-evolved with their specific host plant(s), including wild, non-agricultural plants.”
Once the apoplast is hydrated, it fills with nutrients such as nitrogen and carbon including sugars, amino acids and organic acids that are consumed by the bacteria in much higher quantities than exist in the apoplast of a healthy plant. When the researchers removed the bacteria from the test plants, they measured how much carbon and nitrogen had been taken up in a specific time period. It was six times and 30 times higher, respectively, than that present in the apoplast of an uninfected plant.
“It’s not like the bacteria arrived and ate what was already available,” said Mackey. “Plants are relinquishing sources of carbon and nitrogen into the apoplast, where they are assimilated by the bacteria. Additionally, 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 is, in fact, genetic. Mutant strains of the bacteria created in past studies and lacking WtsE were unable to accomplish the tasks of manipulating water and nutrients.
The study has laid the foundation for future breeding of plants to put the brakes on these bacterial survivalists. Current breeding practices in corn are based on past research focusing on boosting the plants’ immune responses to bacteria.
This study opens up new options for breeders to consider ways to control the ability and virulence of a micro-organism to cause disease. Its virulence is a measure of the severity of damage it can cause.
“By understanding targets that enable the virulence function, breeders could create varieties in which those targets are absent (or non-compatible), which would undermine the virulence activity of these key effectors,” said Mackey.
In addition to corn, the bacteria also infect sudangrass, rice and jackfruit crops in part of the Eastern hemisphere.
“P. stewartii was long thought to be limited to corn and the range of the corn flea beetle,” he said. “But the recent appearance of this bacteria in sudangrass and jackfruit in areas with no corn flea beetles indicates that those assumptions were false. How far and wide can this pathogen spread is an open question.”
Sudangrass is a midsummer grass that is a heat and drought-tolerant cover crop typically grown in the northeast. Jackfruit is a tropical tree fruit grown in south and southeast Asia.
“Other organisms likely deliver the bacteria to those new host plants,” said Mackey. “When it comes to the epidemiology on corn, the severity of disease is tightly correlated with the abundance of corn flea beetles. Cold winters that reduce beetle survival led to low incidence seasons. Insecticides could help but they are not a preferred solution for reasons of both cost and ecological friendliness.”
Mackey said researchers are testing the activities of other AvrE-family members in their host plants to determine the generality of what has been learned from the WtsE protein. The research team will also focus on how WtsE is able to coerce corn to do its bidding and find out which plant proteins the effector hijacks for help. How is it manipulating plant cells? This information will provide valuable information for breeders to develop future Stewart’s wilt resistant varieties.
The research study was published in the journal Cell Host & Microbe.
