One of the most devastating diseases for rice farmers today is the rice blast disease, which creates a yield loss of approximately ten to thirty percent each year—enough rice crops to feed about sixty million people.
This disease, caused by the rice blast fungus Magnaporthe oryzae, is first spread through the wind as spores and latches on tightly to rice plants once in contact with them. Soon after, the spores germinate, and a dome-shaped specialized cell called the appressorium develops. This cell is capable of building up immense amounts of turgor pressure—about eight megapascals, or forty times the pressure of a car tire—which allows it to rupture the leaf’s cuticle. As a result, large lesions begin to form, which spread throughout the plant and eventually kill the crop entirely.
Currently, the only resistance mechanisms used by crop farmers to protect their crops are fungicide sprays and genetically modified rice crops with fungal resistance genes. However, these methods are imperfect, as the rice blast fungus is capable of quickly evolving to overcome any forms of resistance.
However, after six years of study, researchers from the Sainsbury Laboratory, the University of Sussex, the University of Exeter, and the Gregor Mendel Institute of Molecular Plant Biology have recently discovered a sensor kinase used by the fungus to infect the plant.
Before the study, which was led by Lauren Ryder from The Sainsbury Laboratory, the researchers knew that the fungus used osmosis to generate the pressure buildup. The appressorium produces high concentrations of glycerol and water, which then rush in against the concentration gradient. They also knew from a previously conducted study that the rice blast spore produces specialized proteins called septins, which form a ring structure where the appressorium plants its base. These septin protein help generate and guide the force that ruptures the leaf cuticle at a particular point. In this study, the researchers sought to find how the fungus could tell when it had developed sufficient pressure to rupture the cuticle.
To begin, Anotida Madzvamuse, Chandrasekhar Venkataraman, and Vanessa Styles, from the University of Sussex, generated mathematical models that predicted the existence of a turgor sensor, or a sensor that detects when enough pressure has been conjured to puncture the leaf cuticle. Afterwards, the researchers looked at a variety of possible candidates based on the traits they were looking for and eventually found a protein kinase called Sln1 that had the characteristics most similar to that of a turgor sensor. A combination of genetic analysis, cell biological analysis, and mathematical modelling all collectively allowed the researchers to identify Sln1 as the sensor kinase.
“The reason we could tell this was a sensor was because when we deleted the gene encoding this sensor, we found that the appressorium developed these pressure cells and just carried on developing more and more pressure, but they never ruptured the cuticle,” said professor Nick Talbot of the Sainsbury Laboratory.
The research group concluded that this sensor kinase was the key to translating the pressure buildup into a physical force. After the leaf’s cuticle ruptured, the fungus would then grow within the plant until the disease would emerge and new spores would be generated, spreading to other plants and beginning the cycle all over again.
Through this newfound discovery, hopefully more effective fungicides or a more resistant form of the rice plant can be developed to counter this disease.
“We might be able to find inhibitors of it, which could be a new class of fungicides that could be much more environmentally safe. We are very interested in producing things that are sustainable and are much more environmentally friendly. That is one possibility. Another possibility is that we might be able to work on developing rice varieties that are able to resist the plant more effectively. Because they’re either able to have a thicker surface or they may be able to use some other protein type of inhibitor produced in the plant.” concluded Talbot.