Iron acquisition plays a crucial role in fungal pathogenicity. Nematode-trapping fungi (NTFs) serve as important biocontrol agents that can develop traps to capture and kill nematodes. Here, we characterize a non-ribosomal peptide synthase-independent siderophore biosynthetic gene, DhSip1, in NTF Dactylellina haptotyla, which modulates trap (adhesive knob) development and pathogenicity by regulating siderophore-dependent iron acquisition. The deletion of DhSip1 severely impaired adhesive knob formation and reduced nematode mortality. A chrome azurol S assay confirmed that the gene deletion impaired siderophore biosynthesis. Conversely, overexpression of DhSip1 enhanced these phenotypes. Notably, the pathogenicity defects of ΔDhSip1 were fully rescued by exogenous iron rescue assay, supporting a functional link between iron acquisition and adhesive knob-mediated infection. Fluorescence localization revealed specific enrichment of DhSip1 in adhesive knobs during late infection, suggesting that its localization provides a mechanism for local iron enrichment, thereby potentially supporting the formation of adhesive knobs. Collectively, DhSip1 optimizes predatory efficiency by coordinating iron acquisition with adhesive knob development in D. haptotyla. Our work provides new insights into the pathogenicity mechanism of D. haptotyla and establishes a theoretical foundation for biocontrol product development.IMPORTANCEFungal pathogens require iron for pathogenicity, but the role of iron acquisition in Dactylellina haptotyla remains unclear. This study identifies a novel non-ribosomal peptide synthase-independent siderophore synthetase gene, DhSip1, in D. haptotyla, which is essential for siderophore production, iron acquisition, and adhesive knob formation. We demonstrate that iron acquisition critically governs both the adhesive knob development and the pathogenicity of D. haptotyla. Furthermore, DhSip1 mediates local iron enrichment within adhesive knobs, revealing a unique pathogenic mechanism that directly links iron homeostasis to nematode predation. Our findings not only advance our understanding of the pathogenic mechanisms in D. haptotyla but also pave the way for designing effective biocontrol products.
Lei et al. (Mon,) studied this question.