Transcriptome changes in Fusarium verticillioides caused by mutation in the transporter-like gene FST1

Chenxing Niu, Gary A Payne, Charles P Woloshuk

Fusarium verticillioides causes an important seed disease on maize and produces the fumonisin group of mycotoxins, which are toxic to humans and livestock. A previous study discovered that a gene (FST1) in the pathogen affects fumonisin production and virulence. Although the predicted amino acid sequence of FST1 is similar to hexose transporters, previous experimental evidence failed to prove function. Three new phenotypes were identified that are associated with the FST1 mutant of F. verticillioides (Δfst1), namely reduction in macroconidia production, increased sensitivity to hydrogen peroxide, and reduced mycelial hydrophobicity. A transcriptome comparison of the wild type and strain Δfst1 grown on autoclaved maize kernels for six days identified 2677 genes that were differentially expressed. Through gene ontology analysis, 961 genes were assigned to one of 12 molecular function categories. Sets of down-regulated genes in strain Δfst1 were identified that could account for each of the mutant phenotypes. The study provides evidence that disruption of FST1 causes several metabolic and developmental defects in F. verticillioides. FST1 appears to connect the expression of several gene networks, including those involved in secondary metabolism, cell wall structure, conidiogenesis, virulence, and resistance to reactive oxygen species. The results support our hypothesis that FST1 functions within the framework of environmental sensing.