Fusarium graminearum mutants towards identification of pathogenesis-associated molecular patterns

Fusarium graminearum is the primary causal agent of Fusarium head blight disease of cereals. This pathogen causes yield loss and contaminates grains with mycotoxins including deoxynivalenol (DON). It has been previously shown that F. graminearum secretes proteins when grown in DON-inducing medium. Four of these proteins were selected to study candidate elicitors of plant innate immunity. F. graminearum mutants were developed by overexpression (OX) or knockout (KO) of genes that encode these proteins; a translation elongation factor 1A (FgEF1A), ceratoplatanin (FgCP) or two common in fungal extracellular membrane (CFEM) domain containing proteins (FgCFEM-1 and -2). CP is a protein located in the fungal cell walls whereas CFEM is a fungal-specific domain found in some membrane proteins, and both proteins are known to have roles in fungal pathogenesis. OX and KO mutants of these genes are currently being assessed. FgEF1A-KO lines were not generated, but the FgEF1A-OX was shown to have an apparent reduction in pathogenicity compared with the wild-type in both wheat and Brachypodium. This loss in pathogenicity is likely related to the reduced fitness which was observed for this strain (slower mycelial growth and conidial germination compared with the wild-type). A similar reduction in fitness has been reported in yeast in which the EF1A was overexpressed. EF1A is involved in protein translation and its bacterial homologue is a known inducer of plant defence response. FgEF1A-derived peptides are currently being assessed for their ability to activate three pathogenesis-related proteins (glucanase, peroxidase and phenylalanine ammonia lyase) in wheat.