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Genetic defenders protect crops from fungal disease

ing on the mildew species), a second set of genes jumps into the fray. These genes, called EDS1, PAD4, and SAG101, work together in a complex inside the cell, and can signal infected cells to die. By sacrificing these fallen cells, the defense genes can spare healthy ones from infection.

Somerville, Stein, and colleagues at the Max Planck Institute for Plant Breeding in Köln disabled the protective genes in Arabidopsis by introducing mutations, one at a time and in various combinations. They infected these mutants with one of two species of powdery mildew: Blumeria graminis hordei, a species that attacks barley, and Erysiphe pisi, one that thrives on the leaves and pods of pea plants.

"Disabling just three genes allowed the pea powdery mildew to reproduce as well on Arabidopsis as it does on its normal host," Somerville remarked. "Thus, the resistance barriers limiting the growth of inappropriate pathogens are much less complex than expected, relying on just a limited number of genes."

The EDS1, PAD4, and SAG101 gene complex's ability to signal cell death is relatively well known to scientists. However, very little is known about how PEN2 behaves in the cell. The current study demonstrates that the PEN2 protein is a catabolic enzyme--a protein that breaks down other molecules--though its specific target remains unknown.

The study expands on the researchers' previous work with a gene called PEN1. As its name suggests, PEN1 and PEN2 seem to share a common purpose. However, they seem to act via different mechanisms, and PEN2 protects against a wider range of fungal pathogens. For example, Arabidopsis plants with a disabled PEN2 gene are also more susceptible to Phytopthora infestans, the fungus responsible for the notorious Irish Potato Famine of the mid-19th century.

"The resistance mechanisms operating at the cell wall seem to be surprisingly simple," Somerville said. "This suggests it might be possible to reverse engineer cr
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Source:Carnegie Institution


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