Translational evolutionary biology

Translational evolutionary biology

Project 19 May 2021

Antimicrobial resistance is acquired via mutations and/or mobile genetic elements (plasmids and transposons), containing antibiotic resistance genes. 

These mutations and acquired antimicrobial resistance genes can have differing impacts on bacterial fitness (the ability of a bacterium to grow). Multiple mutations and/or mobile genetic elements can interact and alter the fitness landscape of the cell, a process termed epistasis. Additionally these fitness effects are often alleviated via further, compensatory, mutations within the cell. This in turn can lead to collateral sensitivity effects where the development of resistance to one antibiotic alters the sensitivity to another.

We use an in vitro experimental evolutionary approach supported by whole genome sequencing and comparative genomics to characterize these evolutionary trajectories and interactions with the aim of translating these findings into policy and treatment decisions and optimizing the use of antimicrobials in clinical practice.

Currently this work is funded by the MRC and the NIHR.


Recent Articles 

Hubbard ATMet al. Piperacillin/tazobactam resistance in a clinical isolate of Escherichia coli due to IS26-mediated amplification of blaTEM-1B. Nature Communications. 2020. 11 4915 

Hubbard ATMet al. A novel hemA mutation is responsible for a small-colony-variant phenotype in Escherichia coli. Microbiology. 2020. 1-8 

Hubbard ATMet al. Effect of Environment on the Evolutionary Trajectories and Growth Characteristics of Antibiotic-Resistant Escherichia coli Mutants. Frontiers in Microbiology. 2019. 10 1-13 

Podnecky NL, et al. Conserved collateral antibiotic susceptibility networks in diverse clinical strains of Escherichia coli. Nature Communications. 2018. 9 3673