What question did this study set out to answer?

To investigate the role of the Foc4-305 effector in the virulence of Fusarium oxysporum f. sp. cubense and its interactions with host proteins.

March 21, 2026

Fusarium oxysporum f. sp. cubense Race 4 Effector, Foc4-305, Targets a Proline-Rich Protein in Banana and Contributes to Virulence

Key Points

To investigate the role of the Foc4-305 effector in the virulence of Fusarium oxysporum f. sp. cubense and its interactions with host proteins.
Identified effector Foc4-305 through transcriptomic analysis.
Conducted localization studies in Nicotiana benthamiana cells.
Used yeast two-hybrid and coimmunoprecipitation assays to confirm interactions with Ma-PRP.
Performed RNA-seq analysis to compare gene expression in wild-type and knockout mutants.
Deletion of Foc4-305 reduced fungal growth and pathogenicity in banana plants.
Foc4-305 localized in the nuclei and cytoplasm of plant cells.
Virus-induced gene silencing of Ma-PRP increased banana resistance to wilt disease.
Differentially expressed genes associated with growth, stress responses, and host immunity were identified.

Abstract

Fusarium oxysporum f. sp. cubense (Foc) ranks as the leading cause of banana wilt globally, devastating crops through the action of pathogen-secreted effectors. This study revealed Foc4-305 as a putative effector from isolate Foc4, identified via transcriptomics, and validated for its pivotal role in pathogenesis. Deletion of Foc4-305 impaired fungal growth, heightened sensitivity to oxidative stresses and cell wall disruptors, and diminished pathogenicity toward banana plants. Localization studies showed Foc4-305 primarily in the nuclei and cytoplasm of Nicotiana benthamiana cells, where it could inhibit BAX-triggered cell death. Interactions with a proline-rich protein (Ma-PRP) were confirmed through yeast two-hybrid, bimolecular fluorescence complementation and coimmunoprecipitation assays. Western blot analysis showed that Foc4-305 stabilized Ma-PRP proteins in vivo. Virus-induced gene silencing of Ma-PRP enhanced the resistance of bananas to wilt disease. Differentially expressed genes of wild-type Foc4 and effector Foc4-305 knockout mutants were revealed by RNA-seq analysis. GO and KEGG analyses highlighted some of these genes as associated with reproduction, DNA repair, and amino acid metabolism, underscoring the role of Foc4-305 role in enhancing virulence of Foc4 by modulating growth, response to stresses, and involvement in host immunity.

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