Ustilago maydis infection reshapes the maize phyllosphere microbiome through antimicrobial effectors and host metabolic reprogramming

Summary

This mechanistic study reveals how the maize pathogen Ustilago maydis actively suppresses health-promoting phyllosphere bacteria through the antimicrobial effector GH25 whilst simultaneously rewiring host leaf metabolism to favour disease-associated microbiota. Co-inoculation experiments with a GH25-deficient mutant demonstrate that antimicrobial effector activity is functionally linked to fungal virulence, suggesting pathogen-mediated microbiome manipulation is a virulence strategy. The findings integrate molecular pathology with microbial ecology to explain how pathogens exploit host-microbe interactions.

Regional applicability

The study is conducted in a laboratory setting using model pathosystems and does not report field trials or agronomic context in United Kingdom or any specific geography. Findings may inform understanding of smut disease biology globally, but transferability to field conditions and management strategies remains to be determined through applied research.

Key measures

Bacterial community composition and abundance (16S rRNA and culture-based methods); antimicrobial sensitivity of isolated bacterial strains to GH25 effector; fungal virulence in wild-type versus Δgh25 knockout mutants; metabolic potential predictions via genome-scale community models

Outcomes reported

The study characterised how U. maydis infection alters maize leaf bacterial communities, identifying distinct health-associated and disease-associated bacterial groups, and demonstrated that the fungal antimicrobial effector GH25 selectively suppresses health-promoting bacteria whilst host metabolic reprogramming favours disease-associated communities.

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