While the term cell death may at first thought give connotations of an undesirable process, it is actually well known that cell death is an important part of the growth and development of many organisms, including in plants. Intentional cell death is known as programmed cell death, which is an umbrella term for a variety of types of cell death underpinned by different molecular processes. In their recent paper in New Phytologist, Qing Shen and colleagues based in Singapore and China show that an iron-dependent form of programmed cell death is required for the infection process of the major plant pathogen rice blast. Maximising our understanding of the infection process in rice blast will be key for coming up with new ways to tackle this major crop disease in a world very dependent on its target.
Rice blast is a major disease of, you guessed it, rice and is caused by the fungus Magnaporthe oryzae. Its relatives in the Magnaporthe genus cause diseases in other grasses, but rice blast is such a problem that it even has its own devoted international conference. The amount of rice it destroys is estimated as 10-30% of the volume of rice harvested across the world every year, a huge loss of one of the world’s most important grains. As part of the infection process, M. oryzae forms a structure known as an appressorium, which uses a high build up of turgor pressure to penetrate through the cuticle of rice plants and enter the plant cells. It has been reported that cells surrounding the appressorium undergo what appears to be programmed cell death during development of the appressorium. Shen and colleagues find that this programmed cell death is specific type called ferroptosis, which is as the name suggests, iron-dependent. They worked this out by treating the rice blast fungus with an iron chelator (a molecule that sequesters iron) and find that cell death around the appressorium is reduced by it. Several other results confirm further that this is ferroptosis, including that addition of an iron source boosts cell death around the rice blast appressorium.
Inhibiting ferroptosis in the fungus substantially delays penetration and growth of the fungus into the rice plant host, indicating that this programmed cell death is required for the proper function of the appressorium. Application of excess iron to the fungus, by contrast, promoted the growth of invasive structures after penetration. Interestingly, other scientists have recently also linked ferroptosis to defence mechanisms used against rice plants against M. oryzae, of which programmed cell deaths are a well-known part. Following on from this, Shen and colleagues also found that promoting ferroptosis in the host rice plants reduced the spread of the fungus around the penetration site. Iron-dependent cell death is therefore important to both the rice blast fungus for its infection process, and to rice plants for defence against this fungus.
This is a good example of how the same biological process can be used for entirely different purposes in different organisms, and in this case in two organisms that happen to be interacting. The more we understand about how rice blast, and similar pathogens, infect plants and about how plants can fight them off, the more we should be able to do to reduce impact on global agriculture. This is especially important in a time when the world is rocketing towards having 8 billion mouths to feed.