OutlineClick the species name for a description of the organism
Magnaporthe oryzae, the causal agent of rice blast disease, is one of the most devasting threats to food security worldwide. Conservatively, each year enough rice is destroyed by rice blast disease to feed 60 million people (Zeigler et al. 1994). Indeed, the Centers for Disease Control and Prevention has recently recognized and listed rice blast as a significant biological weapon. No part of the world is now safe from this disease. It was long thought of as being confirned to developing nations, but over the past decade it has emerged as a serious problem in the United States. A major epidemic occurred in the Southern US following the widespead introduction of the susceptible cultivar Newbonnet (Marchetti 1994).
The impact of this fungus is beginning to be felt in other ways. Certain strains are able to attack other domesticated grasses, including barley, wheat, pearl millet and turf-grass. Limited outbreaks on wheat have been reported in South America (Valent and Chumley 1994). Widespread devastation of golf courses, particularly in the Midwest, where it has been attacking cool season grasses, is of particular concern (Landschoot and Hoyland 1992).
Cross-section of appressorium of wild Magnaporthe oryzae.
Like many foliar plant pathogens, M. oryzae is well adapted to attack and penetrate its host. All aerial parts of the plant are subject to invasion, but losses are most devastating when the panicle or node at the base of the panicle is infested and killed resulting in loss of grain set (Ou 1985). The infection process is similar to that of many other fungal pathogens and is mediated by the formation of a specialized infection cell, the appressorium (Emmet and Parberry 1975). Although much has been learned, it remains largely a mystery how the emerging germ tube recognizes it is on a suitable surface and sets in motion a series of elaborate development steps that culminate in infection (Dean 1997).
Management of rice blast disease is most precarious (Bonman and MacKill 1988). While in the past, control was mainly through use of expensive and potentially hazardous chemicals (when affordable) the focus has shifted, as it has for most diseases, to more environmentally friendly and potentially less expensive approaches, principally mediated through host resistance. The rice blast genome appears to be quite unstable and in some instances new races appear relatively quickly. A key to developing effective and durable resistance is through a comprehensive understanding of the host-pathogen interaction, which in turn requires a thorough understanding of both the host and the pathogen.
Magnaporthe oryzae is an excellent model organism for studying fungal phytopathogenicity and host-parasite interactions. M. oryzae is a haploid, filamentous Ascomycete with a relatively small genome of ~40 Mb contained in 7 chromosomes (Talbot et al. 1993; Orbach 1996). The majority of fungal pathogens belong to this taxonomic class or exist as related asexual forms (Agrios 1997). M. oryzae is also closely related to the non-pathogen Neurospora crassa, a leading model organism for the study of eukaryotic genetics and biology (Taylor et al. 1993). Unlike many phytopathogenic fungi such as mildews and rusts, the rice blast fungus can be cultured on defined media, facilitating biochemical and molecular analyses. Significantly, early stages of the infection process including germination, appressorium formation and penetration can be studied ex planta (Hamer et al. 1988; Bourett and Howard 1990; Howard and Valent 1996; Dean 1997).
Turf grasses are the most widely cultivated plants, being used for home lawns, urban green space, parks, golf courses and athletic fields. One of most important diseases of turf, and among the most difficult to control, is Summer Patch (or Frog-eye Patch) caused by the soil borne fungus M. poae (Deroeden 1989). Summer Patch is a root disease and affects a number of grasses, including Kentucky bluegrass (Poa pratensis), annual bluegrass (Poa annua), the fescues (Lolium arundinaceum) and creeping bentgrass and occurs wherever susceptible grasses are grown (Jackson 1995). Colonization initiates in root tissues with the first visual signs of disease being 2-6" patches of discolored grass that expand, resulting in straw-colored areas of dead grass measuring up to 12" in diameter. The disease is very hard to control once established. Fungicide applications are only partially effective. They must be sprayed preventatively before symptoms are apparent, and are ineffective unless combined with cultural practices that help to reduce disease severity.
Gaeumannomyces graminis is a necrotrophic soilborne pathogen that colonizes the root and crown tissue of many members of the grass family (Poaceae). G. graminis is a member of the Gaeumannomyces-Phialophora complex of fungi, in which G. graminis represents the haploid homothallic asexual state. It is the most widely distributed of the Gaeumannomyces species and composed of four varieties, the most well known being G. graminis var. tritici, the etiologic agent of take-all disease of wheat and barley, and the most destructive root disease of wheat worldwide (Freeman and Ward 2004). In addition to var. tritici, the three other destructive varieties are: avenae, which causes take-all of oats and take-all patch on bentgrass turf, graminis, which causes black sheath rot of rice, Bermuda grass decline, and take-all root rot of St. Augustine grass (Datnoff et al 1997), and maydis, the causative agent of take-all of maize. Roots of infected plants are invaded by infection hyphae that extend from dark runner hyphae. The infection hyphae produce hyphopodia, attachment and penetration structures similar to the appressoria of M. oryzae.