Differential gene expression to heat stress drives thermotolerance, pathogenicity, and reproduction in Fusarium head blight pathogens: from transcriptomic profiling to functional validation.

backgroundFusarium head blight (FHB) is a destructive wheat disease caused primarily by Fusarium graminearum and F. asiaticum. Climate warming increases the frequency of high-temperature episodes during anthesis, yet the molecular mechanisms underlying thermal adaptation in FHB pathogens remain unclear. Here, we integrated ecological, transcriptomic, and functional approaches to investigate how differential gene expression contributes to heat adaptation and its interplay with virulence and reproduction.

resultsField surveys in Sichuan Province identified naturally occurring strains capable of growth at 34 °C. Comparative transcriptomics revealed extensive differential gene expression under heat stress, with significant enrichment in oxidation-reduction and transmembrane transport processes. Functional validation highlighted two key differentially expressed genes: FgABCF3 (encoding an ABC transporter) and FgSSB1 (encoding a heat shock protein). Deletion of either gene reduced fungal growth at 34 °C, impaired pathogenicity-especially under heat stress-and disrupted sexual reproduction. Overexpression restored wild-type phenotypes. Both genes were markedly upregulated in heat-tolerant strains, confirming their role in thermal adaptation.

conclusionsOur study provides evidence that differential gene expression plays a key role in high-temperature adaptation in FHB pathogens, and is associated with changes in virulence and reproduction. These insights advance our understanding of pathogen evolution under warming climates and highlight potential targets for developing climate-resilient disease management strategies.