COLUMBIA, Mo.– When allergy season comes, plants don’t sneeze and their eyes don’t water, but their immune systems can similarly overreact when they encounter malicious bacteria.

University of Missouri researchers recently observed a previously unknown genetic interaction in a plant’s immune defense that can cause an overactive immune system when it encounters bacterial pathogens. An out-of-control immune system can stunt growth and stifle seed production in a crop.

“When plants turn on their immune system inappropriately, their seed set is often stifled,” said Walter Gassmann, an associate professor of plant sciences in the Christopher S. Bond Life Sciences Center at MU. “In economic terms that’s a big problem.”

Researchers noticed how two proteins can work in tandem, in a process dubbed “cross talk,” to alert the cell to a bacterial invasion.

Special proteins in the plant, called resistance proteins, recognize specific features of bacterial proteins called effector proteins. When a pathogen is detected, a resistance protein triggers an “alarm” that alerts the nucleus of danger. The communications between the resistance proteins and the nucleus are called signaling pathways.

Until now, these signaling pathways were thought wholly separate and not known to “cross talk.”

But Gassmann and his MU colleagues – postdoctoral researchers Sang Hee Kim and Saikat Bhattacharjee, graduate students Fei Gao and Ji Chul Nam, and former undergraduate student Joe Adiasor – found evidence for interaction between two resistance proteins.

The discovery came while studying the immune response of the wild mustard plant Arabidopsis thaliana to the bacterial pathogen Pseudomonas syringae. These bacteria can cause disease, lesions and frost damage in plants. A proper immune response can minimize this harm, but sometimes the immune system doesn’t know when to quit, causing the problems with stunted growth and stifled seed set that Gassmann and his colleagues want to learn how to prevent.

The researchers knew that a resistance protein called RPS4 responds to the P. syringae pathogen. But they discovered that under certain conditions, another resistance protein, SNC1, also joins the fray.

This surprised them because until now this class of plant resistance proteins had been thought to be highly specific, meaning each member responds to a different effector protein. This revelation about cross talk adds an important piece to the puzzle that Gassmann hopes will lead to further insights into plant immune systems.

These results build on many years of research on this mustard plant – a variety developed at MU in the 1960s that is now used in research worldwide – and in the future could contribute to battling pathogen strains that overcome the plant’s immune system.


“When you deploy a single resistance gene in crops, very often it becomes ineffective and you have to come in with the next one,” Gassmann said. “Instead of going one by one, we need to understand the whole network – what is it that the plant recognizes, what is it that the pathogen is trying to manipulate in the host – so we can come up with a truly intelligent way to move or boost immunity in crop plants.”

 Gassmann noted that while their discovery advances understanding of the immune system, much more research is needed.

“We need to understand more than just the tip of the iceberg – which is the resistance gene – but rather how the plant regulates its whole immune system,” he said. “I fully expect that research in molecular plant pathology in the decades to come will be very important to maintain the crop productivity we need to feed people in the face of energy and climate restrictions. I think it is an important piece of future economic productivity.”

The National Science Foundation funded this research, which is reported in the Nov. 4 issue of PLoS Pathogens. Read the journal article here:


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