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Santos-Escobar, F.

Publications and source records attributed to Santos-Escobar, F..

2 recordsLinked to original sources

Stress-Induced Cooperation Promotes Tolerance in Resource-Limited Auxotrophic Microbial Consortia

Microbial communities often rely on metabolic cooperation, especially under nutrient limitation, but how antibiotics influence these interactions remains unclear. Here, we show that exposure to chloramphenicol, a ribosome-targeting bacteriostatic antibiotic, promotes cooperation in auxotrophic Escherichia coli consortia. Using a proteome-partition model, we find that chloramphenicol-induced growth inhibition elevates levels of the alarmone ppGpp, shifting proteome allocation toward amino acid biosynthesis and export. This regulatory response enhances cross-feeding and supports cooperative growth, even under antibiotic stress. Laboratory experiments confirm that, under low amino acid availability, co-cultures of leucine and phenylalanine auxotrophs display greater tolerance to chloramphenicol than monocultures. Both our theoretical and experimental results reveal a feedback loop in which antibiotic stress strengthens metabolic interdependence, buffering growth inhibition and enhancing community-level tolerance.

microbiology↗

Conditional filamentation enhances bacterial survival in toxic environments

Bacterial phenotypic plasticity enables rapid adaptation to fluctuating environments. Filamentation, a shape-shifting response commonly observed under stress, has often been viewed as a byproduct of cellular damage. However, filamentation might also confer survival advantages by influencing toxin accumulation dynamics. In this study, we examined the adaptive value of filamentation in Escherichia coli using a genetically controlled, SOS-independent induction system to compare isogenic, yet phenotypically distinct cells. By integrating mathematical modeling, single-cell microfluidics, and time-resolved flow cytometry, we evaluate bacterial survival under heavy metal and {beta} -lactam antibiotic stress. Our results show that filamentation can improve survival by decreasing the surface area-to-volume ratio, which slows intracellular toxin accumulation and extends the time available for stress response activation or for external toxin levels to dissipate. These findings suggest that filamentation serves as an effective morphological strategy to transiently withstand environmental toxicity, reinforcing its broader role in bacterial stress adaptation.

microbiology↗