Fusarium verticillioides infects maize producing ear rot, yield loss and the accumulation of fumonisins. In the present study, a transcriptomic approach was employed to investigate the molecular aspects of the interaction of susceptible/resistant maize genotypes with fumonisin-producing/nonproducing strains of F. verticillioides over a time course of 4 days after inoculation. The fumonisin-nonproducing strain led transcription in susceptible maize kernels, starting from 48h post inoculation, with a peak of differentially expressed genes at 72h after inoculation. Pathogen attack altered the mRNA levels of approximately 1.0% of the total number of maize genes assayed, with 15% encoding proteins having potential functions in signal transduction mechanisms, and 9% in the category of transcription factors. These findings indicate that signalling and regulation pathways were prominent in the earlier phases of kernel colonization, inducing the following expression of defense genes. In the resistant maize genotype, the fum1 mutant of F. verticillioides, impaired in this polyketide synthase gene (PKS), provoked a delayed and weakened activation of defense and oxidative stress-related genes, compared to the wild-type strain. The inability to infect resistant kernels may be related to the lack of PKS activity and its association with the lipoxygenase pathway. Plant and fungal 9-lipoxygenases had greater expression after fum1 mutant inoculation, suggesting that PKS plays an indirect effect on pathogen colonization by interfering with the lipid mediated cross-talk between host and pathogen.
Keywords: 9-Lipoxygenase gene; Fusarium verticillioides; Microarray; Zea mays.; fum1 mutant.
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