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The Woronin body is a peroxisome-derived dense-core vesicle that is specific to several genera of filamentous ascomycetes, where it has been shown to seal septal pores in response to cellular damage. The Hexagonal peroxisome (Hex1) protein was recently identified as a major constituent of the Woronin body and shown to be responsible for self-assembly of the dense core of this organelle. Using a mutation in the Magnaporthe grisea HEX1 ortholog, we define a dual and essential function for Woronin bodies during the pathogenic phase of the rice blast fungus. We show that the Woronin body is initially required for proper development and function of appressoria (infection structures) and subsequently necessary for survival of infectious fungal hyphae during invasive growth and host colonization. Fungal mycelia lacking HEX1 function were unable to survive nitrogen starvation in vitro, suggesting that in planta growth defects are a consequence of the mutant's inability to cope with nutritional stress. Thus, Woronin body function provides the blast fungus with an important defense against the antagonistic and nutrient-limiting environment encountered within the host plant.
INTRODUCTION
Magnaporthe grisea is an ascomycetous fungus that causes devastating blast disease in graminaceous hosts such as rice (Oryza sativa), wheat (Triticum aestivum), barley (Hordeum vulgare), and millet (Pennisetum americanum). Establishment of excellent molecular genetics for M. grisea makes the rice blast pathosystem a good model for the investigation of fungus-host interactions (Valent, 1990). The disease cycle during a blast infection comprises the following sequence of developmental events: germination of the conidium; sensing of host surface toughness and hydrophobicity by the tip of the germ tube; elaboration of a specialized infection structure called an appressorium; cytoplasmic streaming into the appressorium; build-up of enormous turgor within the appressorium; and forcible entry into the host epidermis through production of an infection peg and subsequent invasive growth in the host tissue. Considerable progress has been made in identifying gene functions necessary for the initial establishment of the fungus on the host (for comprehensive reviews, see Dean, 1997; Tucker and Talbot, 2001; Talbot, 2003), but little is known about the later steps of infection related to invasiveness and in planta fungal growth.
The morphological and physiological transitions during the life cycle of phytopathogenic fungi appear to be induced by the environment encountered...