Bacterial motility can govern the dynamics of antibiotic resistance evolution

Acknowledgements: We thank Kacper Kornet and Deryck Thake from the IT team of the Department of Applied Mathematics and Theoretical Physics of the University of Cambridge for their help with the managing of the supercomputing cluster. We thank Julian Parkhill for discussions about the evolution of antibiotic resistance and for suggesting the study of HGT. We thank Kevin Foster, Oscar Despard, George Fortune, Pierre Haas, Julian Parkhill, Robert Austin, Mike Cates, Nick Barton and Philip Maini for their comments on earlier versions of this manuscript. V.P. was supported by a CMS Summer Research Grant, MI 2022—Oxford Mathematical Institute Scholarship, and had additional support from Gonville & Caius College. N.M.O. was supported by a BBSRC Discovery Fellowship No. BB/T009098/1.Funder: MI 2022 - Oxford Mathematical Institute Scholarship CMS Summer Research GrantSpatial heterogeneity in antibiotic concentrations is thought to accelerate the evolution of antibiotic resistance, but current theory and experiments have overlooked the effect of cell motility on bacterial adaptation. Here, we study bacterial evolution in antibiotic landscapes with a quantitative model where bacteria evolve under the stochastic processes of proliferation, death, mutation and migration. Numerical and analytical results show that cell motility can both accelerate and decelerate bacterial adaptation by affecting the degree of genotypic mixing and ecological competition. Moreover, we find that for sufficiently high rates, cell motility can limit bacterial survival, and we derive conditions for all these regimes. Similar patterns are observed in more complex scenarios, namely where bacteria can bias their motion in chemical gradients (chemotaxis) or switch between motility phenotypes either stochastically or in a density-dependent manner. Overall, our work reveals limits to bacterial adaptation in antibiotic landscapes that are set by cell motility