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NSF Press Release


Embargoed until 5 p.m. EST

NSF PR 02-18 - March 21, 2002

Media contacts:

 Cheryl Dybas, NSF

 (703) 292-8070


 Leslie Lang, UNC-CH

 (919) 843-9687

Program contact:

 Sharman O'Neill

 (703) 292-8070

Protein Plays Espionage Role in Bacterial Attack on Plants

Scientists for the first time have identified a protein that plays a double agent role in the war between plants and disease causing bacteria.

The plant protein, called RIN4, interacts with both invading pathogen molecules, and with another protein from within the plant cell itself, in the plant's disease resistance strategy. The discovery adds important new knowledge to how bacterial pathogens target a host plant's molecular machinery to make it more hospitable, even beneficial, to its plundering invasion.

"This research will increase our understanding of how plant genes mediate resistance to pathogenic bacteria that cause disease and crop losses," says Sharman O'Neill, program director in the National Science Foundation's (NSF) division of integrative biology and neuroscience, which funded the research along with the Department of Energy (DOE).

"This information is likely to lead to novel approaches for pathogen control, and to improved disease resistance in plants. The combination of genetics and biochemistry will allow a unique assault on a disease resistance signaling pathway," said O'Neill.

The research, done at the University of North Carolina at Chapel Hill (UNC-CH), is reported in the March 22 issue of the journal Cell.

"This study is largely about how plants perceive pathogens," said senior study author Jeff Dangl of the UNC-CH school of medicine. "When we study the interaction between host and pathogen, we need to understand it from the pathogen side, including the targets it wants to hit and why, the weapons it uses, and -- on the plant side -- what guard molecules the host deploys."

Dangl and colleagues studied how the wild mustard plant Arabidopsis thaliana responds to Pseudomonas syringae, a bacterial pathogen that also causes diseases in crops like beans, peas and tomatoes. The mustard plant has counterparts of many important human proteins involved in disease, including cystic fibrosis and breast cancer.

The researchers focused on the Arabidopsis disease resistance protein, RPM1, which they previously showed was anchored to the inside of the plant cell membrane. Until now, no one had found a direct interaction between the pathogen's type III effector proteins and the RPM1 receptor. The new study identified such a target, the protein RIN4.

"RIN4 is a protein that bridges between the pathogen-encoded type III disease effector and the plant-encoded disease resistance protein," Dangl said.

When type III effectors are inside the cell, a phosphate is added to RIN4. Dangl and colleagues postulate that this reduces cellular defense. Thus, RIN4 "is normally a negative regulator of defense, and the type III effectors target it and lock it into a negative regulatory mode. Pathogen growth would be facilitated by slowing the host defense response," Dangl said.

But the resistance protein RPM1 appears to serve as a "guard" for cellular proteins that are potential targets of pathogen molecules, like RIN4.

Dangl and other researchers in this field believe that resistance gene products such as RPM1 might be deployed to physically associate with those targets and to intercept the pathogen molecule when it enters the cell.




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