Abstract

Fusarium commune is the main pathogen of lotus rhizome rot, which causes the wilt of many plants. Histone acetyltransferase plays a critical part in the growth and virulence of fungi. In the present study, we identified an FcElp3 in Fusarium commune which homolog histone acetyltransferase Elp3. We further constructed a mutant strain of F. commune to determine the function of FcElp3 in fungal growth and pathogenicity. The results showed the deletion of FcElp3 reulted in reduced mycelial growth and sporulation. Compared with WT, the ΔFcElp3 strain showed more tolerance to osmotic stress and cell wall stress responses, but was highly sensitive to oxidative stress. The subcellular localization results indicated that FcElp3 was distributed in both cytoplasm and nucleus. Western blotting showed that FcElp3 was important for acetylation of H3K14 and H4K8. RNA-seq analysis showed significant transcriptional changes in the ΔFcElp3 mutant with 3098 genes up-regulated and 5770 genes down-regulated. Peroxisome was the most significantly enriched metabolic pathway for down-regulated genes. And it led to a significant decrease in the expression of the core transcription factor Fcap1 involved in the oxidative stress response. Pathogenicity tests revealed that the ΔFcElp3 mutant's pathogenicity on lotus was significantly decreased. Together, these findings clearly demonstrated that FcElp3 was involved in fungal growth, development, stress response, and pathogenicity via the direct regulation of multiple target genes.

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