A pathogenicity cluster for exploiting maize kernels defenses in A. Flavus

Aspergillus flavus is a saprophytic cosmopolitan fungus, capable of infecting crops in pre- and post-harvest exploiting different secondary metabolites, including aflatoxins. The latter are held in high regard as carcinogenic and genotoxic in animals and humans, even though they have no effect on host plants. In mining the genome of A. flavus for identifying secondary metabolite clusters putatively involved in the pathogenesis process, our attention has turned to the cluster 32 containing some fungal effectors such as salicylate hydroxylase, quercetinases and necrosis/ethylene inducing proteins (NepA). In order to understand how this cluster works during the disease, we conducted histological and histochemical experiments in A. flavus pin bar-infected maize caryopses.

The same samples were analyzed for (i) the expression of specific genes inside the cluster (e.g. salOH, NepA), (ii) the production of salicylate and the presence of its dehydroxylated form, i.e. cathecol, by LC-MS/MS.

Within this frame, several mutants of A. flavus impaired or enhanced in specific functions (e.g. cluster 32 overexpression, NepA KO and OE strains) were checked for their ability to cause disease in maize caryopses. A scenario emerged in which fungal progression through living tissues (e.g. aleuron) is accompanied by a significant rise in the level of fungal effectors, such as SalOH and NepA, and by a degradation of SA that, in turn, appears strategic for the fungus to bypass caryopses defences and attenuate programmed cell death phenomena naturally occurring in the aleurone layer of maturating kernels