Abstract
Calcium signalling has profound implications in the fungal infection of plants and animals, during which a series of physiological and morphological transitions are required. In this article, using a model fungal pathogen, Magnaporthe oryzae, we demonstrate that the regulation of the intracellular calcium concentration ([Ca(2+)](int)) is essential for fungal development and pathogenesis. Imaging of [Ca(2+)](int) showed that infection-specific morphogenesis is highly correlated with the spatiotemporal regulation of calcium flux. Deletion of the fungal phospholipase C gene (M. oryzae phospholipase C 1, MoPLC1) suppressed calcium flux, resulting in a fungus defective in developmental steps, including appressorium formation and pathogenicity. Surprisingly, the PLC-delta1 gene of mouse was able to functionally substitute for MoPLC1 by restoring the calcium flux, suggesting the evolutionary conservation of the phospholipase C-mediated regulation of calcium flux. Our results reveal that MoPLC1 is a conserved modulator of calcium flux that is essential for the regulation of key steps in fungal development and pathogenesis.