The cereal pathogen Fusarium graminearum threatens food and feed production 
worldwide. It reduces the yield and poisons the remaining kernels with 
mycotoxins, notably deoxynivalenol (DON). We analyzed the importance of 
gamma-aminobutanoic acid (GABA) metabolism for the life cycle of this fungal 
pathogen. GABA metabolism in F. graminearum is partially regulated by the global 
nitrogen regulator AreA. Genetic disruption of the GABA shunt by deletion of two 
GABA transaminases renders the pathogen unable to utilize the plant stress 
metabolites GABA and putrescine. The mutants showed increased sensitivity 
against oxidative stress, GABA accumulation in the mycelium, downregulation of 
two key enzymes of the TCA cycle, disturbed potential gradient in the 
mitochondrial membrane and lower mitochondrial oxygen consumption. In contrast, 
addition of GABA to the wild type resulted in its rapid turnover and increased 
mitochondrial steady state oxygen consumption. GABA concentrations are highly 
upregulated in infected wheat tissues. We conclude that GABA is metabolized by 
the pathogen during infection increasing its energy production, whereas the 
mutants accumulate GABA intracellularly resulting in decreased energy 
production. Consequently, the GABA mutants are strongly reduced in virulence 
but, because of their DON production, are able to cross the rachis node.