Death and chemotaxis: Bacterial chemotaxis enables collective escape from phage predation
7 affiliations
- 1Department of Chemical and Biological Engineering, Princeton University, Princeton, NJ 08544, USA.
- 2Department of Chemical and Biomolecular Engineering, University of Delaware, Newark, DE 19716, USA.
- 3Princeton Center for Theoretical Science, Princeton University, Princeton, NJ 08544, USA.
- 4Department of Physics, Princeton University, Princeton, NJ 08544, USA.
- 5Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ 08544, USA.
- 6Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
- 7Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
Abstract
Bacteriophages ("phage") are viruses that prey on bacteria in diverse environments, from biological tissues to soils. In many of these environments, bacterial hosts are constantly migrating, yet how bacterial migration is influenced by phage predation remains poorly understood. Using transparent granular hydrogels that mimic natural habitats, we directly visualize populations of motile Escherichia coli encountering lytic T4 phage. Unexpectedly, we find that even in phage-rich environments, bacteria successfully form chemotactic fronts that enable them to migrate over large distances without necessarily requiring new phage resistance mutations. At low phage concentrations, the front is indistinguishable from a phage-free control, and the population remains largely susceptible; at higher concentrations, the susceptible population initially collapses, and the front is reestablished by a less susceptible subpopulation enriched under intense predation. Higher phage concentrations delay front formation but not steady-state front speed or shape. By combining our experiments with biophysical modeling, we demonstrate that this phenomenon reflects a competition between collective chemotactic migration and phage predation, quantified by a dimensionless "escape parameter," in which sufficiently rapid migration allows the population to outpace the spreading infection. This work thus provides mechanistic insight into how cell motility shapes phage-bacteria interactions in spatially extended environments.
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BibTeX
@article{muir2026death,
title = {{Death and chemotaxis: Bacterial chemotaxis enables collective escape from phage predation}},
author = {Victoria G. Muir and Alejandro Martínez-Calvo and Ned S. Wingreen and Sujit S. Datta},
journal = {Science Advances},
year = {2026},
month = oct,
doi = {10.1126/sciadv.aeg2358},
url = {https://www.science.org/doi/10.1126/sciadv.aeg2358},
note = {CC BY},
}
RIS
TY - JOUR
TI - Death and chemotaxis: Bacterial chemotaxis enables collective escape from phage predation
AU - Victoria G. Muir
AU - Alejandro Martínez-Calvo
AU - Ned S. Wingreen
AU - Sujit S. Datta
PY - 2026
DA - 2026/10/16
JO - Science Advances
DO - 10.1126/sciadv.aeg2358
UR - https://www.science.org/doi/10.1126/sciadv.aeg2358
AB - Bacteriophages ("phage") are viruses that prey on bacteria in diverse environments, from biological tissues to soils. In many of these environments, bacterial hosts are constantly migrating, yet how bacterial migration is influenced by phage predation remains poorly understood. Using transparent granular hydrogels that mimic natural habitats, we directly visualize populations of motile Escherichia coli encountering lytic T4 phage. Unexpectedly, we find that even in phage-rich environments, bacteria successfully form chemotactic fronts that enable them to migrate over large distances without necessarily requiring new phage resistance mutations. At low phage concentrations, the front is indistinguishable from a phage-free control, and the population remains largely susceptible; at higher concentrations, the susceptible population initially collapses, and the front is reestablished by a less susceptible subpopulation enriched under intense predation. Higher phage concentrations delay front formation but not steady-state front speed or shape. By combining our experiments with biophysical modeling, we demonstrate that this phenomenon reflects a competition between collective chemotactic migration and phage predation, quantified by a dimensionless "escape parameter," in which sufficiently rapid migration allows the population to outpace the spreading infection. This work thus provides mechanistic insight into how cell motility shapes phage-bacteria interactions in spatially extended environments.
SN - 2375-2548
ER -