The histone acetyltransferase FocGCN5 regulates growth, conidiation, and pathogenicity of the banana wilt disease causal agent Fusarium oxysporum f.sp. cubense tropical race 4.

Chromatin structure modifications by histone acetyltransferase are involved in multiple biological processes in eukaryotes. In the present study, the GCN5 homologue FocGCN5 was identified in Fusarium oxysporum f. sp. cubense tropical race 4 (Foc TR4). The coding gene was then knocked out to investigate the roles of FocGNC5. The mutant ΔFocGCN5 was found significantly reduced in growth rate and conidiation, and almost completely lost pathogenicity to banana plantlets. The RNA-seq analysis provide an insight into the underlying mechanism. Firstly, transcription of the genes involved in carbohydrate metabolism and fungal cell wall synthesis was reduced in ΔFocGCN5, leading to the impairment of apical deposition of cell-wall material. Secondly, FocabaA, one of the pivotal regulators of conidiation, was significantly reduced in expression in ΔFocGCN5, which might be the main cause of the conidiation reduction. Thirdly, the pathogenicity-associated factors, including effectors and plant cell wall degrading enzymes, were almost all down-regulated in ΔFocGCN5, which accounts for the decrease of pathogenicity. In addition, the stress tolerance to salt, heat, and cell wall inhibitors was slightly increased in ΔFocGCN5. Taken together, our studies clarify the roles of FocGCN5 in growth, conidiation, and pathogenicity of Foc TR4, and explore the possible mechanism behind its biological functions.