Black death or black rot: U-M scientists find plant and animal bacteria share same deadly cell-killing mechanism

ANN ARBOR---When it comes to killing cells, Yersinia pestis---the bacterium that causes bubonic plague---is the stealth assassin of the pathogen world. It kills quietly and efficiently by first slipping inside immune system sentinel cells and cutting off the communication lines they need to call for help.

Now scientists at the University of Michigan have discovered the molecular mechanism Yersinia uses to sever these vital cell signaling pathways. It turns out to be an ancient agent of death---so effective that both plant and animal bacteria have been using it throughout long periods of evolutionary history.

Results from the U-M study---completed in collaboration with scientists at the University of California-Berkeley, the State University of New York at Stony Brook and Brookhaven National Laboratory---are published in the Nov. 24 issue of Science.

"YopJ, the protein Yersinia uses to cut cell signaling pathways, is one of six proteins the bacterium injects into immune cells called macrophages," says Jack E. Dixon, Ph.D., the Minor J. Coon Professor of Biological Chemistry in the U-M Medical School and co-director of the U-M's Life Sciences Institute. Every Yop has a specific function and they work together to get inside cells and destroy the body's defense systems.

In research published last year in Science, Dixon's team reported that YopJ attacks two vital cellular signaling pathways called MAPK and NF(B, which regulate immune response and help prevent cell death.

"Now we have found closely related variants of YopJ in several species of pathogenic plant and animal bacteria, as well as in Rhizobium---symbiotic bacteria that live on plant roots," says Dixon, who directed the research project.

When Mary Beth Mudgett, Ph.D., a postdoctoral fellow at the University of California-Berkeley
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Contact: Sally Pobojewski
pobo@umich.edu
734-647-1844
University of Michigan
22-Nov-2000