Plant pathogenic bacteria cause high crop and economic losses to human societies^1-3. Infections by such pathogens are challenging to control as they often arise through complex interactions between plants, pathogens and the plant microbiome^4,5. This natural ecosystem is rarely studied experimentally at the microbiome-wide scale, and consequently we poorly understand how taxonomic and functional microbiome composition and the resulting ecological interactions affect pathogen growth and disease outbreak. Here we combine DNA-based soil microbiome analysis with in vitro and in planta bioassays to show that competition for iron via secreted siderophore molecules is a good predictor of microbe-pathogen interactions and plant protection. We examined the ability of 2150 individual bacterial members of 80 rhizosphere microbiomes, covering all major phylogenetic lineages, to suppress the bacterium Ralstonia solanacearum, a global phytopathogen capable of infecting various crops^6,7. We found that secreted siderophores altered microbiome-pathogen interactions from complete pathogen suppression to strong facilitation. Rhizosphere microbiome members with growth-inhibitory siderophores could often suppress the pathogen in vitro, in natural and greenhouse soils, and protect tomato plants from infection. Conversely, rhizosphere microbiome members with growth-promotive siderophores were often inferior in competition and facilitated plant infection by the pathogen. Because siderophores are a chemically diverse group of molecules with each siderophore type relying on a compatible receptor for iron uptake^8-12, our results suggest that pathogen-suppressive microbiome members produce siderophores the pathogen cannot use. Altogether, our study establishes a causal mechanistic link between microbiome-level competition for iron and plant protection and opens promising avenues to use siderophore-mediated interactions as a tool for microbiome engineering and pathogen control. 

Source data for Figures 1-4 and Supplemental Figures 1-6 from the associated paper.