Resistance to Fusarium verticillioides and fumonisin accumulation in maize inbred lines involves an earlier and enhanced expression of lipoxygenase (LOX) genes.

Fusarium verticillioides causes ear rot in maize and contaminates the kernels with the fumonisin myco-toxins. It is known that plant lipoxygenase (LOX)-derived oxylipins regulate defence against pathogensand that the host-pathogen lipid cross-talk influences the pathogenesis. The expression profiles of fif-teen genes of the LOX pathway were studied in kernels of resistant and susceptible maize lines, grownin field condition, at 3, 7 and 14 days post inoculation (dpi) with F. verticillioides. Plant defence responseswere correlated with the pathogen growth, the expression profiles of fungal FUM genes for fumonisinbiosynthesis and fumonisin content in the kernels. The resistant genotype limited fungal growth andfumonisin accumulation between 7 and 14 dpi. Pathogen growth became exponential in the susceptibleline after 7 dpi, in correspondence with massive transcription of FUM genes and fumonisins augmentedexponentially at 14 dpi. LOX pathway genes resulted strongly induced after pathogen inoculation in theresistant line at 3 and 7 dpi, whilst in the susceptible line the induction was reduced or delayed at 14 dpi.In addition, all genes resulted overexpressed before infection in kernels of the resistant genotype alreadyat 3 dpi. The results suggest that resistance in maize may depend on an earlier activation of LOX genesand genes for jasmonic acid biosynthesis.