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Study illuminates how the plague bacteria causes disease

ing cell shape, Stebbins said.

Mutations that prevented the bacterial proteins' interaction with the host protein significantly impaired YpkA's ability to disrupt the cytoskeleton. Moreover, a mutant strain of Y. pseudotuberculosis that lacked the GDI activity caused significantly fewer problems for infected mice compared to normal bacteria.

"Earlier studies that focused only on the protein's kinase activity had missed half the picture," Stebbins said. "The GDI domain seems to have an even bigger effect on host cells in culture, and a significant impact on virulence."

The results also add to broader themes in the evolution of bacterial diseases, the researchers added.

"It is becoming increasingly clear that a common strategy used by bacterial pathogens to manipulate host cell biology is the mimicry of their own biochemical processes," Stebbins said.


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Source:Cell Press


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