Reveals how dynamic acetylation of a metabolic enzyme impacts spore germination, indicating its role in host infection.
Fungal spores maintain viability and then germinate to infect host plants, but how these biological processes are integrated remains elusive. Here, we show that γ-carboxymuconolactone decarboxylase 1 (FolCmd1) is an acetylated protein reversibly regulated by the controlling enzymes in the devastating soil-borne pathogen Fusarium oxysporum . FolCmd1 is largely acetylated and imported into the nucleus by FolFkbp4, thereby avoiding excessive metabolism of aromatic amino acids that are critical for long-term survival of spores. During invasion, FolCmd1 is deacetylated and translocated into the cytoplasm to remove host-derived ferulic acid, thus enabling spore germination. Consequently, dysacetylation of FolCmd1 leads to impaired virulence. These findings reveal a sophisticated pathogenic mechanism by coordinating two developmental stages through dynamic modification of a metabolic enzyme.
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Yang et al. (2026) studied this question.
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