UK researchers engineer plant immunity against devastating blast fungus

Every year, a fungus called Magnaporthe oryzae destroys enough rice to feed sixty million people. It is the most destructive disease of cultivated rice on Earth. In recent decades, it has jumped to wheat and barley, spreading through parts of Asia and Africa with a speed that has alarmed researchers and policymakers watching global food supplies. A changing climate means it could eventually reach northern Europe, including the United Kingdom, where it does not yet exist. Against this backdrop, a team of scientists at the John Innes Centre in the UK, working with colleagues at Kobe University in Japan, has identified a new molecular pathway that might allow them to engineer crops with stronger, more durable defenses against the pathogen.

The blast fungus survives by inserting molecular tools called effectors into plant cells. These effectors are like tiny saboteurs—they slip into the leaf and stem cells of rice, wheat, and barley, then manipulate the plant's own biology to promote infection and spread. Plants, however, have evolved their own countermeasures. They possess receptors that recognize these foreign effectors as threats and trigger an immune response. When the alarm sounds, the plant kills its own infected cells to prevent the pathogen from advancing further through the tissue. For more than three decades, plant scientists have focused their attention on one particular class of these immune receptors, called nucleotide-binding and leucine-rich receptors, or NLRs. They have been the foundation of our understanding of how plants fight blast and other diseases.

In recent years, researchers have begun investigating a second class of immune receptors that was only recently discovered in cereals. These are called tandem kinase proteins, or TKPs. What makes TKPs interesting is that some of them contain an integrated domain—a specific structural feature—known as a heavy metal-associated, or HMA, domain. This same type of domain has been found in some NLR receptors, and it appears to play a crucial role in recognizing pathogen effectors and mounting an immune response. Mark Banfield, a professor and group leader at the John Innes Centre, saw the potential immediately. "If we can engineer these integrated HMA domains for new properties by making amino acid protein changes where effectors bind, we can gain what we call novel recognition specificities—and potentially a new front line for defense of plants against disease," he said.

The research team used advanced techniques—biophysical analysis and crystallography—to map out, at high resolution, exactly how HMA domains interact with blast pathogen effectors at the molecular level. They discovered that HMA domains function as biological baits, luring the pathogen's effectors into a trap. Armed with this structural knowledge, the researchers then took a significant step: they successfully bioengineered TKP immune receptors to have dual specificity. In other words, they engineered the receptors to recognize and bind to effectors associated with infection of both wheat and barley—something that does not occur naturally. The findings were published in Science Advances.

The experiments were conducted using protoplasts, individual wheat cells isolated and used as stand-ins for whole plant tissue. These proof-of-principle demonstrations show that TKPs are amenable to bioengineering in ways that might have seemed impossible just a few years ago. Dr. Daniel Yu, the study's first author, noted that the team's success with TKPs suggests that the engineering tools previously developed for NLR receptors may also work with this newer class of immune proteins. The next phase of work will move beyond isolated cells to greenhouse plants, testing whether the engineered receptors function as intended in living tissue.

The implications extend beyond a single crop or a single pathogen. Banfield and his colleagues believe that TKPs and NLRs may activate immunity through different mechanisms. That difference could be the key to building crops with more robust, harder-to-defeat defenses. "We think these two classes of immune receptors are probably activated in different ways," Banfield explained. "That gives the potential for more robust immunity in the field because you are not putting all your eggs in one basket." The team envisions a future in which multiple defense genes—encoding both TKPs and NLRs—could be stacked together in the same crop, creating what Banfield calls a super-resistant plant. Because the two receptor classes would activate immunity through distinct pathways, it would be far more difficult for the pathogen to evolve resistance to both simultaneously. Precision breeding and artificial intelligence tools may accelerate this work, helping scientists design novel specificity into HMA domains with greater speed and accuracy. For now, the research has cleared a conceptual hurdle: it has shown that a new class of plant defense proteins can be engineered, refined, and potentially combined to create crops that can withstand one of agriculture's most persistent threats.