Scientists from Nanyang Technological University (NTU) in Singapore have identified a key mechanism by which the dangerous plant bacteria Xanthomonas can infect crops. The Xanthomonas bacteria, known as the “crop killer,” is a globally prevalent bacterium capable of infecting 400 different plant species. Citrus canker is caused by the bacterial pathogen Xanthomonas citri subsp.
The NTU researchers identified the exact cellular-level mechanism by which the bacteria can penetrate and hijack a plant’s immune system and leave it vulnerable to infection.
The study, led by Miao Yansong and Yu Jing, has important implications for food safety and sustainability. The findings were published in the journal Nature Communications in July.
“Xanthomonas is a plant pathogen that infects a variety of plants, including food crops, so understanding this mechanism is important for controlling crop diseases,” said Yansong.
The researchers successfully reverse-engineered the infection mechanism and obtained a provisional patent for a “toolkit” that may help in the development of new methods to make plants more resistant against bacteria.
The Xanthomonas bacteria infects and damages plants by injecting toxic effector proteins into the plant host. These toxic effector proteins hijack and take over the plant’s normal biological processes, preventing them from mounting an immune response.
Plants normally resist infection at the cellular level using a protective layer of plasma membrane to shield their actin cytoskeletons, which serve as the structure of a cell. During a successful infection, the pathogen breaks through the membrane and overwrites the cytoskeleton with new instructions telling it not to fight it.
The NTU team studied a specific type of effector protein called XopR, which behaves like a molecular glue. They discovered that XopR hijacks the host cytoskeleton by undergoing what is called a liquid-liquid phase separation process on the surface of the plant’s plasma membrane.
This phase separation process is similar to the way that oil and water can merge into each other, yet can also be easily separated into two distinct liquids. Both the XopR protein and the host plant cell interact with each other like liquid droplets, allowing the toxic effector proteins to “glue” onto the plant cell and merge into it.
Once this has happened, the interconnected XopR proteins can infiltrate and invade the plant cell’s actin cytoskeleton network, giving it access to cell behavior. When this happens, the XopR protein can overwrite the existing cellular instructions to mount an immune response, thus leaving the plant vulnerable to infection.
“Our study was not only a biological study of bacteria protein, but also about the biochemistry behind the infection mechanism,” Yu Jing said. “By studying the physico-chemical properties of XopR liquid droplets, we were able to further understand its unique protein sequence. This interdisciplinary approach allowed us to reveal the underlying molecular mechanisms by which XopR subverts the immunity of its plant host.”
This newly discovered mechanism of how effector proteins hijack plant cells through phase-separation can be broadly applied to other plant-pathogen interactions and provides new avenues for future research.
Source: Nanyang Technological University
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