Soybean safety lies in strange genetic sequence

Plant scientists from the University of Wisconsin-Madison have determined the sequence of genes which confer resistance, when duplicated, to soybean cyst nematode (SCN) infection. In terms of the effect on yield, SCN is one of the most serious diseases to affect soybean, which is an important source of protein and oil for many people across the globe.

The study, which appeared this week in the journal Science, is the result of a collaborative effort between Professor Andrew Bent from the Department of Plant Pathology at the University of Wisconsin-Madison, graduate student David Cook, and others including the University of Illinois’ Matthew Hudson. It demonstrates that the repetition of a particular three-gene structure known as Rhg1 effectively protects soybean plants from the nematodes.

Although soybean has been bred to contain copies of Rhg1 for many years – indeed this is the preferred method of protecting crops against the cyst nematode – it requires multiple copies of the sequence to confer resistance and very little is known about the mechanisms at work. I spoke to Professor Bent to find out more about the work he and his colleagues have been doing, as well as the work that remains to be done…

How does the soybean cyst nematode affect soybean and why is it such a difficult disease to control?
SCN saps energy from the plant, often without the plant showing any outward signs of distress. The nematode feeding sites are areas of high metabolic activity, and a single infested root system can have over a hundred little nematodes feeding on it. 

There are many reasons why the disease is difficult to control. The nematode cysts are a hearty survival structure. Roughly half of the nematode eggs that form on a crop will hatch by the end of the next year, but a substantial portion hatch in subsequent years, across an entire decade. This means that once a field is infested there is a very persistent source of inoculum.

Those pesticides which work well against nematodes are very expensive to apply and are generally used only on higher-value crops like strawberries or potatoes. Growers almost always prefer to use plants with inherent disease resistance as the main disease control method, but for SCN the available resistance is not complete. The Rhg1 locus provides very good disease control, but not complete protection from SCN, so the nematodes persist as a disease problem.

How do your new findings build on previous work aimed at developing resistant soybean?
The Rhg1 locus that we characterised at the molecular level has been in use for many years on millions of soybean acres. At many stages of soybean breeding, plant breeders already use DNA tests of neighbouring genes to predict the presence of desirable versions of Rhg1, as an alternative to expensive SCN testing. It may be immediately useful that our work offers DNA markers to directly detect the different versions of the Rhg1 genes, rather than making predictions based on nearby genes. However, the more exciting prospect is to use these findings to identify or create more effective versions of Rhg1. Some versions of Rhg1 work better than others against certain nematode populations, for example, and there is great interest in addressing that issue.

What is unusual about the discovery that multiple copies of Rhg1 confer resistance?
Having multiple copies of a gene can offer the chance for evolutionary changes in one copy, while another copy is preserved to carry out the original function; that is very common across all organisms. But a few things are unusual about Rhg1.

First, the SCN resistance trait is conferred by at least three genes at the Rhg1 locus rather than one gene; those genes are all right next to each other, a trait common in microbes but not in multicellular organisms.

Second, this small block of genes is not just duplicated; it is present in as many as ten adjacent copies in the SCN-resistant plants.

Lastly, it appears that the SCN resistance trait is a matter of higher expression of these genes, achieved by this gene copy number increase, rather than being due mainly to amino acid differences between the encoded proteins of resistant and susceptible plants, or due to transcription factors that raise the expression of any given copy of the genes. 

How much do we know about the mechanism(s) at work here?
We still know very little about the biochemical mechanisms of resistance. Now that we have discovered the relevant genes, we are turning our attention to those questions. With three genes to study, we may have supplied ourselves with three times as much work! Two of the three gene products appear to be involved in trafficking molecules within or between cells, so that is a starting point. We also are curious to study genetic and evolutionary mechanisms, asking how this genetic structure arose, and whether it changes readily.

What are the next stages for your research? Could there be implications for other diseases?
The previous answers address a few interesting areas: biochemical mechanisms, genetic mechanisms, and also the variable efficacy of Rhg1 against different nematode populations. But your question anticipates another idea we are testing: can the Rhg1 genes be placed into other plants to potentially control other cyst nematode diseases? More broadly, can the cellular/biochemical themes of Rhg1-mediated resistance be adapted to work against other nematode diseases? There is a need for many more scientists than our lab can furnish to explore all of these questions.