Pathogenesis and Genome Organization of the Rice Blast Fungus

Abstract

Plant diseases caused by fungi present a serious challenge to our efforts to feed the world’s rapidly increasing population. Manipulation of plant genes through genetic engineering and traditional breeding provides an opportunity to improve the disease resistance in crops of agricultural significance. In addition, the application of target-based drug design will lead to the identification of various novel chemical agents that will possess significant potential as disease control agents. The success of such approaches will depend heavily on the biological knowledge of fungal pathogens in such areas as mechanisms of virulence and pathogenicity, population structure and dynamics, and the nature and mechanisms of genetic changes underpinning the evolution of new races. As a result of limited resources, coupled with the necessity to study many fungal diseases of economic significance, comprehensive research focused on these aspects of fungal biology has been restricted to a limited number of model systems. Magnaporthe grisea, the causal agent for rice blast disease, has become one such system. Worldwide, rice blast is one of the most economically devastating crop diseases. In addition to its agricultural significance, the rice blast system presents many advantages as an experimental model: (a) Extensive genetic and molecular analyses of host specificity and pathogenicity have been carried out; (b) Molecular and cellular bases of infection processes are well characterized; (c) Rice is a model genetic system for monocots; (d) Well-saturated genetic and physical maps of M. grisea are available; (e) Genome sequencing of both rice and M. grisea is in progress; (f) Genetic and race diversity of fungal populations in many rice-growing areas has been extensively surveyed. In this chapter we aim to provide an overview of the nature of the interaction between M. grisea and its hosts and the corresponding mechanisms employed at each level, from molecules to populations.