Gene expression profile of MAP kinase PTC1 mutant exposed to deoxynivalenol

Abstract

Deoxynivalenol (DON) is a secondary metabolite that is generated by Fusarium species, which seriously affects both humans and livestock. Protein synthesis inhibition and ribotoxic stress, caused by induction of the mitogen activated protein kinase (MAPK) cascade, are thought to be responsible for the majority of DON toxicity. However, as DNA damage has also been reported, it is necessary to clarify all sources of toxicity. In this study, we conducted a DON exposure test using the PTC1 yeast mutant with disrupted MAPK-related genes, and observed gene expression changes using DNA microarray analysis. Our results indicated changes in the expression of genes associated with protein synthesis inhibition, as well as with DNA damage. At the same time, genes related to the synthesis of folic acid, a coenzyme in DNA synthesis, were inhibited. To complement the dysfunction of these genes, the growth media was supplemented with folic acid. As a result, the recovery of growth was confirmed, although it was a consistent effect and it did not reflect differences in susceptibility to DON toxicity.

かび毒の細胞に対する毒性評価と産生菌検出に関する研究

“…Results from each study showed that the toxicity of each mycotoxin generally aligned with that reported for animal cell systems, indicating that yeast cells can be used as an easy-to-handle eukaryotic cell evaluation system. For the evaluation of AFB 1 , the Saccharomyces cerevisiae BY4743 ptc1 mutant strain, lacking the beta-1,3-glucan synthesis gene, was used [4]. This mutation results in the loss of repressive control of the mitogen-activated protein kinase pathway, indirectly altering the expression of phosphoenolpyruvate carboxykinase, leading oxaloacetate in the tricarboxylic acid (TCA) cycle to the glycogenic pathway.…”