1.10.3S
SIGNAL TRANSDUCTION AND MORPHOGENESIS DURING MAGNAPORTHE GRISEA INFECTION

J HAMER, K ADACHI, T BHARGAVA, JIN-RONG XU and M URBAN

Purdue University, West Lafayette, USA

Background and objectives
A wide diversity of parasitic fungi form infection structures when in contact with plant hosts. Such structures almost always differentiate from the tips of growing germ tubes, which use a tactile sensing mechanism called thigmotropism to initiate infection structure differentiation. The rice blast fungus differentiates an appressorium when asexual spores are germinated in contact with hard hydrophobic surfaces such as plastic films or coverslips. However when spores are germinated on agar surfaces they produce the mycelial network typical of filamentous fungi. A central question in fungal biology is: how do fungal pathogens sense appropriate surfaces for differentiating infection structures?

Results and conclusions
A variety of experimental approaches have been taken in order to answer this question in the rice blast fungus. Importantly, gene-replacement mutagenesis has been used to assess the role of various gene products in appressorium formation. Thigmotropic sensing appears to involves a cell-surface protein called Mpg1. This protein has characteristics of a ubiquitous family of fungal surface proteins called hydrophobins [1]. Once an appropriate surface is encountered, signalling involves the activation of adenylate cyclase (Mac1) via a heterotrimeric G protein [2]. The cAMP-mediated signal-transduction pathway ultimately results in the activation of protein kinase A (PKA). This signalling pathway is also needed for growth, sexual morphogenesis and asexual sporulation. Studies of mutations in the regulatory subunit of PKA suggest that divergent signalling for growth and pathogenesis appears to be accomplished at the level of activation of PKA regulation. A mitogen-activated protein (MAP) kinase called Pmk1 is also specifically required for appressorial differentiation [3]. Another MAP kinase, designated MPS1, is required for appressorial penetration. Although MPS1 mutants fail to penetrate plant cells, they are able to elicit early plant defence responses including autofluorescence, cytoplasmic streaming and rearrangments in the plant actin cytoskeleton. Studies of the temporal pattern of defence gene expression in rice confirm that M. grisea can activate the plant defence response prior to penetration of the plant cell.

References
1. Talbot NJ, 1995. Trends in Microbiology 3, 9-16.
2. Liu S, Dean RA, 1997. Molecular Plant-Microbe Interactions 10, 1075-1086.
3. Xu J-R, Hamer JE, 1996. Genes and Development 10, 2696-2706.