Antifungal Proteins that Mediate Host Plant Defense Against Pathogens


Model fungal genetic systems are being used for molecular genetic dissection of antifungal protein function. We have determined that the plant antifungal protein, osmotin, interacts with a receptor on the cell wall/membrane that initiates a MAP kinase signal transduction pathway that results in cell death. This research is defining the fundamental mechanisms by which plant defensive proteins are fungicidal.

Osmotin, A Plant Antifungal Protein, Subverts Signal Transduction to Enhance Fungal Cell Susceptibility

Molecular Cell (In Press)

Summary - The plant pathogenesis-related protein, osmotin, is an antifungal cytotoxic agent that causes rapid cell death in the yeast Saccharomyces cereviseae. We shoe here that osmotin uses a signal transduction pathway to weaken defensive cell wall barriers and increase its cytotoxic efficacy. The pathway activated by osmotin includes the regulatory elements of the mating pheremone response STE4, STE18, STE20, STE5, STE11, STE7, FUS3, KSS1, and STE12. Neither the pheremone receptor nor its G protein alpha-subunit GPA1 are required for osmotin action. However, mutation of SST2, a negativ regulator of Galpha proteins, resulted in super-sensitivity to osmotin. Phosphorylation of STE7 was rapidly stimulated by osmotin preceding any changes in cell vitality or morphology. These results demonstrate that osmotin subverts target cell signal transduction as part of its mechanism of action.

Figure legend. Model for the Signal Transduction Pathway in Osmotin-Induced Cell Death. Osmotin treatment activates a MAPK cascade that shares the components STE20, STE11, STE7, KSS1 and STE12 with the the pheremone response, invasive and pseudohyphal growth pathways and additionally, STE4, STE5, FUS3 and STE18 with the pheremone response pathway. We propose that osmotin subverts another existing MAPK cascade, with unidentified natural stimulus, by a process that may or may not require a Galpha protein and a receptor. Activation of this cascade induces changes in the cell wall that facilitate osmotin access to the plasma membrane and consequently, cell death.




Last Update: 04/27/98