New research reveals how insect-transmitted bacteria can make some flowering plants sterile, turning them into what botanists are calling “zombie plants.”
It's hard to imagine a horror film about zombie plants. For a start, running away sounds rather easy. However, in actuality, the phenomenon of bacteria overtaking plants can have disastrous economic consequences. That’s because the bacteria makes the plants produce leaves instead of flowers. “Broom growth,” as the condition is known, threatens many crops, including popular grape varieties.
"Insects transmit bacteria, so-called phytoplasmas, which destroy the life cycle of the plants," said Professor Günter Theißen of Friedrich Schiller University Jena in a statement. "These plants become the living dead. Eventually they only serve the spread of the bacteria."
In Trends in Plant Science, Theißen and his student Florian Rümpler studied the protein SAP54, an essential part of the process. "This protein comes from the bacteria and bears a strong structural resemblance to proteins which form a regulatory complex inside the plant, which permits a normal development of the blossom," said Rümpler.
The authors conclude that SAP54 is so similar to the plants' MADS-domain-proteins that other proteins in the plant bind to SAP54 rather than the ones they need to. This interferes with normal functioning, turning the plants sterile and reducing them to the growing dead.
“Plant MADS-domain-proteins subdivide into different subfamilies with different functions and different binding preferences of their K-domains due to small alterations in their amino acid sequence. The K-domain of each subfamily is 'fine-tuned' to specifically bind to a defined subset of K-domains belonging to other subfamilies,” Rümpler said to IFLScience. “SAP54 specifically binds to just a small subset of MADS-domain proteins. It is not the interaction strength but the interaction specificity that makes SAP54 so effective.”
Theißen and Rümpler were intrigued as to how the bacteria managed to make a protein that fits its targets so perfectly. "It is conceivable that both proteins trace back to a common origin," Rümpler said. "However we suspect that this is not the case." Instead, the pair think the bacteria's protein started out with a coincidental weak match, and natural selection did the rest.
There are some plants that seem to have evolved defenses against it, since a few varieties are resistant, but Rümpler said no mechanism is known at this point. Worse still, he told IFLScience, his work doesn't lead to any obvious path for protecting vulnerable trees.
“As the targeted plant proteins are incorporated in a very complex interaction network, all alterations that may allow the protein to escape binding of SAP54 will most likely result in unfavorable side effects,” Rümpler said to IFLScience.
The saddest thing is that the phytoplasmas may not even benefit from their destruction. “The sterility of the plant itself is not known to be beneficial for the bacteria,” Rümpler told IFLScience. However, the leafhoppers that spread the disease are preferentially attracted to affected plants and, Rümpler said, “Some studies showed a slightly positive effect on the [leafhoppers'] lifespan” when they feed on affected leaves.