Tobias Bollenbach

The paper shows that combining biotin biosynthesis inhibition with metformin reduces Pseudomonas aeruginosa virulence and restores antibiotic sensitivity by targeting metabolic pathways.

The paper quantifies fitness costs of protein overexpression in E. coli, showing growth collapse due to membrane proteome displacement, not translocation pathway saturation.

The paper develops a generalized growth law to predict antibiotic interactions by integrating single-drug responses and showing how different antibiotics affect ribosome levels and growth.

This study shows that function-specific epistasis shapes antibiotic resistance evolution, with some genetic backgrounds leading to novel resistance trajectories and slower resistance development.

The paper investigates how intra- and extracellular β-lactamase activity contributes to collective β-lactam survival in E. coli under cefotaxime stress.

This study identifies how competition and protection in microbial communities influence resistance evolution, using mathematical models and experiments with E. coli and M. liquefaciens.

This paper introduces PHORCE, a method to quantify phage amplification rates and reveals wide variation in phage-antibiotic interactions across Escherichia coli phages.

This study shows that adding trace elements to chemically defined media reduces variability in microbial growth experiments, supporting their routine use for more reproducible results.

The paper shows introns in yeast RP genes induce phenotypic heterogeneity under osmotic stress, providing a fitness advantage by enabling differential survival strategies during starvation.

The paper investigates drug interactions between translation-inhibiting antibiotics by modeling them as translation bottlenecks and shows how kinetic factors and continuous epistasis influence these interactions.