Fumonisins are toxic secondary metabolites produced by the maize pathogens Fusarium verticillioides and F. proliferatum, agents of pink ear rot; and by some strains of F. oxysporum and Aspergillus niger. The fumonisin biosynthetic enzymes and accessory proteins are encoded by a set of clustered and co-transcribed genes collectively named FUM, whose molecular regulation is beginning to be unraveled. In fungi in general, gene expression is often partially controlled at the chromatin level in secondary metabolism; physical clustering is thought to favor this process. Epigenetic regulation of FUM genes was indeed proven; namely the deacetylation/acetylation of histones on the promoter regions of some key genes was shown to control their expression level in F. verticillioides. We are at present investigating the molecular underpinnings of this phenomenon, by generating hdf1 mutants of F. verticillioides. FvHdf1 is the putative homolog of the class II histone deacetylase FgHdf1 of F. graminearum, which contributes most to wild-type mycotoxin production in this fungus; our hypothesis is that among other effects, FUM expression is de-regulated in the Fvhdf1 mutants. Also, we are exploring the possibility of a direct connection between oxylipin metabolism and the chromatin state at FUM loci, through the characterization of the epigenetic marks on FUM genes in F. verticillioides mutants with altered oxylipin levels. Preliminary results on these mutants will be presented.
Investigating the epigenetic regulation of Fumonisin biosynthesis in Fusarium verticillioides
VISENTIN, IVAN;CARDINALE, Francesca
2012-01-01
Abstract
Fumonisins are toxic secondary metabolites produced by the maize pathogens Fusarium verticillioides and F. proliferatum, agents of pink ear rot; and by some strains of F. oxysporum and Aspergillus niger. The fumonisin biosynthetic enzymes and accessory proteins are encoded by a set of clustered and co-transcribed genes collectively named FUM, whose molecular regulation is beginning to be unraveled. In fungi in general, gene expression is often partially controlled at the chromatin level in secondary metabolism; physical clustering is thought to favor this process. Epigenetic regulation of FUM genes was indeed proven; namely the deacetylation/acetylation of histones on the promoter regions of some key genes was shown to control their expression level in F. verticillioides. We are at present investigating the molecular underpinnings of this phenomenon, by generating hdf1 mutants of F. verticillioides. FvHdf1 is the putative homolog of the class II histone deacetylase FgHdf1 of F. graminearum, which contributes most to wild-type mycotoxin production in this fungus; our hypothesis is that among other effects, FUM expression is de-regulated in the Fvhdf1 mutants. Also, we are exploring the possibility of a direct connection between oxylipin metabolism and the chromatin state at FUM loci, through the characterization of the epigenetic marks on FUM genes in F. verticillioides mutants with altered oxylipin levels. Preliminary results on these mutants will be presented.
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