Chlorate is converted by the nitrate reductase to toxic chlorite, and therefore it can be used as an indicator for nitrate reductase activity. Indeed, reduced growth rates in presence of chlorate for the bcvel1 loss-of-function mutants were found indicating the up-regulation of the nitrate-metabolizing enzymes also under axenic conditions. Like other necrotrophic plant pathogens, B. cinerea produces complex secondary metabolites exhibiting phytotoxic activities, e. g., the botryanes and the botcinins. Noteworthy, B05.10 and T4 isolates were previously shown to differ in their potential to form these compounds: while both groups of toxins are produced by B05.10, T4 only produces botrydial-like toxins. VeA homologues are described as global regulators of secondary metabolite gene clusters in diverse fungi, and in fact, the impairment of secondary metabolism by deletion of the VeA homologue affects virulence in some but not all pathogens producing toxic compounds. Hence, fumonisin-deficient F. verticillioides Dfvve1 mutants cause symptomless endophytic infections when plants were grown from inoculated seeds, and loss of thrichothecene and T-toxin production in F. graminearum and C. heterostrophus mutants, respectively, is accompanied by reduced virulence. In contrast, the deletion of VeA in D. septosporum resulted in reduced formation of dothistromin but not in reduced virulence. Therefore, we had hypothesized an impact of the bcvel1 deletion on the formation of the two known groups of toxins. Surprisingly, the production of both toxins was not affected by the bcvel1 deletion in strain B05.10, neither in vitro nor in planta. Currently, only these two metabolite groups have been investigated in detail by functional and chemical analyses. However, the genome of B. cinerea comprises approximately 40 genes encoding key enzymes of secondary metabolism, such as polyketides, nonribosomal peptides and terpenes. Some of these B. cinerea-specific genes are highly expressed during infection of sunflower cotyledon, grape berries or bean leaves and one of them, bcpks7, appeared to be BcVEL1-dependent. However, whether the corresponding metabolites are associated with virulence remains to be investigated. Oxalic acid is a compound that is produced by numerous filamentous fungi, including the A. niger, A. fumigatus and the plant pathogens B. cinerea and S. sclerotiorum. Although OA is derived from primary metabolism, it can be considered as a secondary metabolite as it is not required for the survival of the organisms but it might be associated with the pathogenic lifestyle in some fungi. Thus, the loss of OA formation in S. sclerotiorum results in nonpathogenic mutants, while an OA-deficient B. cinerea strain is still able to infect plant tissues. The different impact of OA on virulence of both fungi might be associated with different pH dynamics during plant tissue colonization. Billon-Grand and coworkers recently showed that S. sclerotiorum R428 decreases the ambient pH value and remained in an acidic environment while B. cinereacolonized tissue established a final neutral environment after temporary lowering the pH at 48 hpi. The increase of the pH value in B. cinerea-infected tissue can be assigned to a much lower OA formation accompanied by an enhanced formation of ammonia while in S. sclerotinia-infected tissues both OA and ammonia formation increase simultaneously maintaining acidic conditions. OA is a versatile compound that may modulate fungus-host interactions in different ways.