Loss of heterochromatin protein 1 (Hep1) in Fusarium graminearum leads to hypervirulence and mycotoxin overproduction during pathogenic growth.

Upon axenic cultivation in presence of the mycotoxin inducing nitrogen source L- ornithine the HEP1 deletion mutant showed an altered secondary metabolite profile including reduced levels of deoxynivalenol (DON). This finding was contrasted with a 1.5 fold increased infection rate on the susceptible wheat cv. Remus which was accompanied by increased production of DON. Transcriptome analysis of the HEP1 deletion versus the PH-1 wildtype strain during pathogenic growth state as well as during saprophytic growth on dead (non-responding) wheat heads and axenic samples allows to distinguish gene response of the pathogen reacting on signals from the active, defending plant from those regulated by plant substrate effects or in vitro mimicked mycotoxin inducing conditions, providing insights into gene regulation underlying the observed hypervirulence. Overall design: Three different growth conditions with two to three replicates