Functional complementation of fumonisin biosynthesis in FUM1-disrupted fusarium verticillioides by the AAL-toxin polyketide synthase gene ALT1 from Alternaria alternata f. sp. Lycopersici

Abstract

Fumonisins and AAL-toxins are mycotoxins produced by several widespread fungal pathogens of crops. The carbon backbone of the mycotoxins originates from a highly reduced, acyclic polyketide, a C18 chain for fumonisins and a C16 chain for AAL-toxins. Fungal reduced polyketides are assembled by iterative modular polyketide synthases (PKS), and their biosynthetic mechanism is not very clear. Here, we cloned the PKS gene, ALT1, from the tomato pathogen Alternaria alternata f. sp. Lycopersici and introduced it into Fusarium verticillioides 5777, which does not produce fumonisins due to a disrupted fumonisin PKS gene, FUM1. An ALT1 transformant of strain 5777 produced fumonisin B series as well as fumonisin analogues. The results provide experimental evidence for the function of ALT1, which encodes a PKS for mycotoxin biosynthesis. The results also show that the C16-synthesizing ALT1 is able to support the C18 fumonisin biosynthesis in F. verticillioides, suggesting that the final size of the fungal reduced polyketides is not determined by the PKSs alone. Unlike other PKSs, these PKSs do not have a thioesterase/cyclase domain. The release of polyketide precursors that are covalently attached to the PKSs involves a distinct mechanism, which probably determines the structure of the final products.