Calcium/calmodulin-dependent signaling for appressorium formation in the plant pathogenic fungus Magnaporthe grisea

Magnaporthe grisea, the causal agent of rice blast, forms a dome-shaped melanized infection structure, an appressorium, to infect its host. Environmental cues that induce appressorium formation by this fungus include hydrophobicity and hardness of contact surface, and chemicals from the host. To determine if the calcium/calmodulin-dependent signaling systems are involved in appressorium formation in M. grisea, we tested the effects of the calcium chelator, calcium ionophore, diverse intracellular calcium modulators, and calmodulin antagonists on appressorium formation. Several calcium modulators and calmodulin antagonists inhibited appressorium formation at the microM level, while conidia germination remained unaffected. There was an inhibition of appressorium formation by EGTA, a calcium chelator, which was restored by the addition of exogenous CaCl2. Neomycin, a phospholipase C inhibitor, specifically inhibited appressorium formation at concentrations from 10 microM to 100 mM. These data suggest that a calcium/calmodulin-dependent signaling system is involved in the appressorium formation of M. grisea.