Quinolone-mediated metabolic cross-feeding develops aluminium tolerance in soil microbial consortia

Aluminium (Al)-tolerant beneficial bacteria confer resistance to Al toxicity to crops in widely distributed acidic soils. However, the mechanism by which microbial consortia maintain Al tolerance under acid and Al toxicity stress remains unknown. Here, we demonstrate that a soil bacterial consortium composed of Rhodococcus erythropolis and Pseudomonas aeruginosa exhibit greater Al tolerance than either bacterium alone. P. aeruginosa releases the quorum sensing molecule 2-heptyl-1H-quinolin-4-one (HHQ), which is efficiently degraded by R. erythropolis. This degradation reduces population density limitations and further enhances the metabolic activity of P. aeruginosa under Al stress. Moreover, R. erythropolis converts HHQ into tryptophan, promoting the synthesis of peptidoglycan, a key component for cell wall stability, thereby improving the Al tolerance of R. erythropolis. This study reveals a metabolic cross-feeding mechanism that maintains microbial Al tolerance, offering insights for designing synthetic microbial consortia to sustain food security and sustainable agriculture in acidic soil regions. The mechanism of soil microbial consortia resistant to aluminium toxicity is unclear. Here, the authors show that the quorum sensing signaling molecular HHQ produced by one member of the consortium can server as the nutritional resource for the other consortium member for aluminium tolerant cell wall component synthesis.