A NIFA-funded research team led by Dr. Andrew Bent at the University of Wisconsin uncovered the molecular mechanism of a very widely used soybean trait for cyst nematode resistance. The findings, published in this week’s online early edition of PNAS, will be useful in developing soybean varieties with increased resistance to the most economically damaging soybean disease.
Soybean cyst nematode resistance is encoded by Rhg1, a tandemly repeated gene cluster within the soybean genome encoding proteins that are essential to normal cell function. Soybean cyst nematodes rely on normally functioning soybean cells to be able to trick the cell machinery into making feeding sites that support nematode growth.
But how can a mutation in a soybean gene required for normal cell function be detrimental to the nematode without being detrimental to the plant? Bent’s team found that resistant soybeans have both resistance-conferring (mutant) and standard genes encoding this protein. The version of the protein that impairs normal cell function becomes more abundant at soybean cyst nematode feeding sites, preventing nematode growth. Meanwhile, the normally functioning version of the protein dominates throughout the rest of the plant, enabling normal cell function and plant growth.
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