Rice blast disease: hopes for control

Prof Nick Talbot, FRS

This is a guest post by Prof Nick Talbot, FRS, Deputy Vice Chancellor for Research and Knowledge Transfer of the University of Exeter. You can follow him on Twitter @talbotlabexeter

Readers of PlantVillage (www.plantvillage.com) will be well aware of the devastation that plant diseases can cause, whether they are affecting garden produce or agricultural fields, the symptoms of plant diseases are very obvious from blights and rusts, to moulds and mildews.

The devastation reeked by plant pathogens also makes a huge impact on the ability of the world to feed itself. It has recently been estimated that losses due to plant pathogens are one of the most significant constraints on worldwide food production. Indeed, it has been estimated that if normal, low-level plant diseases could be effectively controlled, this would allow food production sufficient to feed 8.5% of the current human population (almost 600 million people). Therefore to ensure global food security, we will require more durable means of controlling plant diseases, and we have to do that in a more sustainable way that is less heavily dependent on fossil fuels, and does not adversely affect the environment, including human health. This is a big challenge and will take considerably greater understanding of plant diseases and the pathogens that cause them.

Where I work, at the University of Exeter (www.ex.ac.uk) , we are researching a wide variety of plant pathogens including major diseases of wheat, barley, maize and rice (http://biosciences.exeter.ac.uk) . Among these, the most significant from an economic perspective and humanitarian viewpoint is the devastating rice blast pathogen Magnaporthe oryzae. Each year, rice blast disease claims between 10–35% of the global rice harvest, this is more than enough rice to feed 60 million people, and if even a fraction of the losses caused by rice blast could be alleviated in a sustainable manner then this would have an enormous impact on global food security.

The world population is growing rapidly and this is particularly true in Asia, where more than 80% of rice is both grown and consumed. In fact, rice production must double by 2030 in order to feed the world’s growing population. Rice blast is, however, a difficult challenge to overcome. The disease occurs wherever rice is grown and exhibits some amazing biology, which enables this highly specialized pathogen to gain entry to plants and cause such a persistent and devastating disease.

Rice blast infections start when three-celled spores, called conidia, land on the surface of a rice leaf and quickly germinate to produce a polarised germ tube, which then differentiates into a special infection structure called an appressorium. The appressorium is essentially a pressure cell. It develops really enormous pressure, estimated to be up to 8.0 MegaPascals (this equates to 80 bars of pressure or almost 80 atmospheres!). Turgor is focused as physical force to puncture the tough rice cuticle. Understanding this process, which involves rapid changes in physiology of appressoria to bring about this enormous turgor generation, is pivotal to developing modern, environmentally safe fungicides that might be developed to control rice blast disease. Once the rice blast fungus has gained entry into the plant cells it undergoes further developmental changes, in which it forms specialised feeding hyphae, which colonise plant tissue and rapidly colonise whole leaves. After only four days, disease symptoms appear and these form large dead spots, or necrotic lesions on the surface of rice leaves, from which the fungus will sporulate (for life cycle see http://www.exeter.ac.uk/nicktalbot/lifecycle/) . Spores are washed or blown to new rice leaves, starting the cycle again and leading to rapid spread of the disease.

Figure 1. Rice Blast Disease caused by the filamentous fungus Disease lesions on 21-day-old rice (seedlings. The disease appears 4–5 days after spores land on the leaf surface.

Rice blast disease is currently controlled either by application of fungicides– which are both expensive and very difficult for growers in the developing world to afford –or by deployment of disease resistance genes. In both cases controlling rice blast is problematic, because the fungus is highly variable and continues to evolve new specific races, which can overcome resistance genes deployed in the field after only two to three growing seasons. Identifying novel sources of rice blast resistance from rice germplasm collections, such as the collections at the International Rice Research Institute (http://irri.org/about-us/our-mission) , or other grass species, is therefore critical to our long terms prospects of controlling rice blast disease. If these disease resistance genes can be deployed in more favourable combinations, in high yielding elite rice cultivars, then the resulting plants will be much more resistant to attack. However, this approach requires more detailed knowledge of both the fungus and its host.

Neck Blast Symptoms. Photograph taken by the author in Hunan Province in China in 2007, showing devastating neck blast symptoms. The fungus attacks the stem of rice, leading to loss of the panicle that holds rice grain. This leads to more than 80% yield loss

In my research group at Exeter, we are trying to understand the biology of Magnaporthe oryzae from the moment the fungus arrives on a rice leaf to the development of disease symptoms. To do this, we are identifying and characterising genes and the biological processes they control. For instance, we now know that turgor is the result of solutes, including glycerol, accumulating to very high concentrations in appressoria (paper here). This draws water into the cell generating high pressure. We also know that when the pressure cell forms, the spore from which it originally developed must die by a form of programmed cell death (paper here) . This allows the recycling of its contents to the appressorium, providing the energy to fuel turgor generation and the cellular changes needed for plant infection (paper here). The challenge now is to take these discoveries and apply them to develop novel means of stopping the fungus from gaining entry to plants. We are trying to do this by finding inhibitors of these processes, that could work very specifically to control rice blast.

We, like many other teams around the world, are also trying to understand how the fungus manipulates its plant host, suppressing the normal immune response of rice, and thereby proliferating within rice tissue. Magnaporthe possesses large numbers of proteins called effectors, which are secreted by the fungus (paper here) and enter plant cells. These proteins suppress plant immunity (paper here) and interfere with the mechanisms that rice has evolved to recognise and defend itself from the fungus. Characterising these effectors is important. Not only to reveal the ways in which fungi can suppress plant immune responses, but because the effectors themselves can be targeted by plant disease resistance proteins. Indeed, this is the main way that plants evolve new resistance to diseases. Knowing the whole effector repertoire of a pathogen therefore provides a means of identifying new plant disease resistance genes, which are valuable in agriculture and can be deployed by plant breeders or new GM varieties. If different effectors can be screened on large germplasm collections (paper here), then it provides the ability to define completely new resistance genes that can then be deployed to control disease more effectively. Deploying new resistance gene combinations is a major aim of plant pathology research worldwide (paper here).

At Exeter, we are currently undertaking a project that is funded by BBSRC, DFID and the Bill and Melinda Gates Foundation as part of the Sustainable Crop Production for International Development programme. This project is aimed at developing durable resistance to rice blast disease in sub-saharan Africa. Our aim is to understand the population biology of the rice blast fungus and the diversity found in Kenya, Uganda, Burkina Faso and other countries throughout the region. We will then characterise the effector repertoire of M. oryzae isolates, by using a combination of next generation DNA sequencing and testing of isolates against the international differential set of rice cultivars carrying each major resistance gene known to rice blast disease. We will also test a wide range of African cultivars grown within the region, including high yielding New Rice for Africa (NERICA) cultivars developed by AfricaRice (http://www.africarice.org ) .

The overall goal of the project is to develop an efficient method to breed for improved disease resistance, based on the knowledge we are gaining about diversity of the rice blast fungus population in Africa. The project involves a truly international team and is an exciting challenge for us at Exeter. Prof. Tom Mitchell and Prof. Guo-Liang Wang from Ohio State University, provide expertise in pathogen genomics and rice blast resistance, respectively. Prof. Jim Correll from the University of Arkansas is carrying out resistance assessment and also overseeing the collection of all of our rice blast populations in Africa. In Kenya, a group led by Dr Lusike Wasilwa at KARI are collecting and cataloguing rice blast strains, which is primarily being carried out by my PhD student David Mwongera Thuranira who is there for most of 2014. A repository for rice blast isolates is being developed at BecA-ILRI by Dr Jagger Harvey and in Burkina Faso, Dr Ibrahima Ouédraogo is overseeing rice blast collections, along with Dr Patrick Okori at Makerere University. Once we have evaluated the overall spectrum of virulence of the rice blast population, we will identify the resistance genes in rice that offer the chance of excluding the largest proportion of the indigenous population of the fungus. These will be pyramided using marker-assisted breeding, which is already in progress in Ohio State and Arkansas, using three of the most promising resistance genes. We have over 100 M. oryzae isolates from Kenya that we are pathotyping in Exeter, in a project led by Dr Lauren Ryder and my PhD student Vincent Were, along with genome sequencing and effector definition of a set of these isolates.

If this project can achieve even half of its ambitious aims in the next four years, then we will have made a significance advance in understanding and developing new disease control strategies for rice blast in a region of the world where it really matters from a societal and humanitarian standpoint. It is the chance to make such a difference that motivates me and the members of my research group to study rice blast disease.

If you are interested in learning more about rice blast, then visit my web-site (http://www.exeter.ac.uk/nicktalbot/).

Official Twitter account of http://t.co/PTia9K3R

Official Twitter account of http://t.co/PTia9K3R