Many fungal pathogens penetrate plant leaves from a specialized cell called an appressorium. The rice blast pathogen Magnaporthe gnsea can also penetrate synthetic surfaces such as poly (vinyl chloride). Previous experiments have suggested that penetration requires an elevated appressorial turgor pressure. In the present report we have used nonbiodegradable Mylar membranes, exhibiting a range of surface hardness, to test the proposition that penetration is driven by turgor. Reducing appressorial turgor by osmotic stress inhibited penetration of these membranes. The size of the turgor deficit required to inhibit penetration was a function of the surface hardness. Penetration of the hardest membranes was inhibited by small decreases in appressorial turgor, while penetration of the softer membranes was sensitive only to large decreases in turgor. Similarly, penetration of the host surface was inhibited in a manner comparable to penetration of the hardest Mylar membranes. Indirect measurements of turgor, obtained through osmotically induced collapse of appressoria, indicated that the infection apparatus can generate turgor pressures in excess of 8.0 MPa (80 bars). We conclude that penetration of synthetic membranes, and host epidermal cells, is accomplished by application of the physical force derived from appressorial turgor.The mechanism of host surface penetration by plant pathogenic fungi has been debated for nearly a century (1-6). The potential role of extracellular enzymes, to facilitate perforation of the host cuticle or cell wall during fungal invasion, is poorly understood (with one exception) due to the complex and ill-defined chemical nature of plant surfaces (7). On the other hand, an essential role for mechanical force during host surface penetration has been proposed for the rice blast fungus Magnaporthe grisea (Hebert) Barr (8). This pathogen produces unicellular infection structures, called appressoria, which adhere tightly to the host surface and produce slender infection pegs that pierce the underlying cell wall. The cell walls of appressoria contain a dense layer of pentaketidederived melanin whose presence is correlated with a build-up of appressorial turgor pressure (8) and is essential for penetration (8,9). In this study, we have inhibited penetration by exposing appressoria to solutions of high osmotic pressure. This approach was used to reduce the hydrostatic pressure (or turgor) within the infection apparatus and to estimate the magnitude of the turgor involved in penetration. Our results offer unequivocal evidence for an extraordinary mechanical component of the mechanism by which appressoria penetrate hard surfaces, but do not exclude a role in host penetration for some other factor such as extracellular enzymes. MATERIALS AND METHODSOrganism and Growth Conditions. These studies were conducted with strain 042 (see ref. 8) of M. grisea (Hebert) Barr, telomorph of Pyricularia grisea Sacc. (10). The time course of infection-structure development in vitro has been well documented ...

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