Opposing functions of Fng1 and the Rpd3 HDAC complex in H4 acetylation in < i > Fusarium graminearum < /i >

In this study, we identified the ortholog of the human inhibitor of growth (ING1) gene inF.graminearum (FNG1) and found that it specifically interacts with the FgEsa1 HAT of the NuA4 complex. Deletion ofFNG1 led to severe growth defects and blocked conidiation, sexual reproduction, DON production, and plant infection. Thefng1 mutant was normal in H3 acetylation but significantly reduced in H4 acetylation. A total of 34 spontaneous suppressors offng1 with faster growth rate were isolated. Most of them were still defective in sexual reproduction and plant infection. Thirty two of them had mutations in orthologs of yeastRPD3,SIN3, andSDS3, three key components of the yeast Rpd3L HDAC complex. Four mutations in these three genes were verified to suppress the defects offng1 mutant in growth and H4 acetylation. The rest two suppressor strains had a frameshift or nonsense mutation in a glutamine-rich hypothetical protein that may be a novel component of the FgRpd3 HDAC complex in filamentous fungi. FgRpd3, like Fng1, localized in euchromatin. Deletion ofFgRPD3 resulted in severe growth defects and elevated H4 acetylation. In contract, theFgsds3 deletion mutant had only a minor reduction in growth rate butFgSIN3 appeared to be an essential gene. RNA-seq analysis revealed that 48.1% and 54.2% of the genes with altered expression levels in thefng1 mutant were recovered to normal expression levels in two suppressor strains with mutations inFgRPD3 andFgSDS3, respectively. Taken together,...
Source: PLoS Genetics - Category: Genetics & Stem Cells Authors: Source Type: research