A. San Millan

This study shows that β-lactamase expression in E. coli induces collateral sensitivity to colistin and azithromycin, suggesting a therapeutic strategy to counter mobile AMR.

The paper identifies promoter activity in gene-less cassettes from Vibrio superintegrons, showing they enhance downstream cassette expression and confer antibiotic resistance.

The paper deletes a chromosomal integron in Vibrio cholerae and shows it has no detectable effect on physiology, proving its genetic and functional isolation.

This study investigates the fitness effects of the plasmid pOXA-48 in clinical enterobacteria using CRISPR-Cas9 to cure plasmids, revealing mostly neutral effects with rare fitness costs or benefits.

The paper investigates how antimicrobial resistance levels and conjugation permissiveness influence plasmid distribution in clinical enterobacteria, showing that specific bacterial clones stabilize plasmid spread.

This study shows that multi-copy plasmids in E. coli generate antibiotic heteroresistance through copy number variability, enabling transient resistance and population regeneration.

This study tracks the evolution of plasmid-mediated antimicrobial resistance in hospitalized patients, revealing trade-offs between resistance levels and bacterial fitness.

This study examines the fitness effects of CTX-M-15-encoding IncF plasmids in E. coli ST131 H30Rx hosts, finding moderate fitness costs in some strains but not others.

The study determines the distribution of fitness effects for plasmid pOXA-48 in gut bacteria, showing quasi-neutral effects and beneficial effects in some isolates, and links plasmid persistence to bacterial diversity and phylogeny.

This study investigates collateral sensitivity associated with antibiotic resistance plasmids, showing its conservation in clinical isolates and potential for selective elimination of plasmid-carrying bacteria.

This study characterizes the dissemination routes of the carbapenem resistance plasmid pOXA-48 in a hospital setting using mechanistic models and genomic data.

This study shows genetic dominance influences the evolution and spread of mobile genetic elements in bacteria by favoring dominant mutations and silencing recessive alleles in horizontally transferred genes.