Abstract
BACKGROUND: Fusarium proliferatum, a globally distributed phytopathogen causing destructive root rot in economically vital crops, employs epigenetic mechanisms to adapt to environmental conditions. RESULTS: Our genome-wide characterization identified eight histone deacetylase (FpHDACs) genes phylogenetically classified into RPD3/HDA1 and Sirtuin subfamilies. Comprehensive genomic characterization revealed two distinctive features: expanded domain architectures exemplified by the Arb2domain within Fp_HDA1, and subcellular localization prediction indicates-where most FpHDACs reside cytoplasmically under neutral pH, but undergo nuclear translocation in alkaline environments. Evolutionary diversification occurred principally via subfunctionalization rather than gene duplication, evidenced by non-clustered chromosomal distribution (8 genes across 5 chromosomes), divergent gene architectures in intron-exon organization and CDS lengths, and promoter cis-element enrichment featuring combinatorial stress-responsive signatures, most notably the dehydration-responsive DRE motifs exclusive to Fp_HOS3. Expression profiling analysis reveals a conserved global suppression of FpHDACs under abiotic stress, which is markedly potentiated by histone deacetylase inhibitor treatment. Crucially, the observed suppression was counterbalanced by a context-dependent induction of Fp_HOS3-specifically triggered under oxidative and cell wall stress, but not by other stressors. This specialized isoform functions as a compensatory epigenetic modulator, fine-tuning stress responses through targeted histone modification. CONCLUSION: This study provides the first systematic elucidation of the HDAC gene family's core structural and functional characteristics in F. proliferatum, yielding novel insights into the adaptive strategies-both conserved and innovative-that underpin fungal stress epigenetics.