Biology subjects

Ehrmann, A. K.

Publications and source records attributed to Ehrmann, A. K..

3 recordsLinked to original sources

bioRxiv2026

Pushing for survival: Spatial intermixing and indirect resistance enable collective growth

The survival of bacterial communities depends on complex dynamics at molecular, cellular, and ecosystem levels. Understanding antibiotic resistance requires a broader community context, as emergent dynamics can lead to unexpected outcomes, such as the persistence of susceptible populations or community collapse. We capture these behaviors by integration of microscopy and mathematical modeling to understand how bacterial interactions and spatial organization shape bacteriostatic antibiotic resistance in a two-strain community. We show that local chloramphenicol detoxification and mechanical pushing shape bacterial coexistence and spatial organization, promoting the survival and growth of otherwise susceptible bacteria. Additionally, the timing of antibiotic administration critically determines the growth dynamics, co-existence, local diversity of susceptible and resistant bacteria, and overall community resistance. Together, these insights highlight how community-level interactions fundamentally reshape antibiotic responses and open new avenues to understand and control bacterial resilience. SIGNIFICANCE STATEMENTAntibiotic resistance is usually treated as a property of individual bacterial strains, yet bacteria typically grow in dense, spatially structured communities where physical interactions matter. We find that under bacteriostatic (growth pausing) antibiotic stress, resistant bacteria can create highly localized protective environments that allow sensitive cells to survive and proliferate. This protection arises not only from antibiotic detoxification, but also from growth-driven mechanical pushing that maintains close cell-cell proximity. As a result, antibiotic tolerance emerges as a collective, spatially dependent property rather than an intrinsic trait of single cells. These findings show that spatial organization, physical forces, and treatment timing can strongly reshape therapy outcomes, with implications for how resistance is understood and managed in microbial communities.

biophysics↗

bioRxiv2025

Wrinkles emerge from matrix complementarity in heterogenous biofilms

Biofilms are dynamic communities of microorganisms encased in a self-produced extracellular matrix. These resilient structures pose challenges across nearly all human activities, from healthcare to industry. The mechanical behaviour of a biofilm is shaped by the heterogenous composition of its matrix, both spatially and chemically. In turn, these mechanics influence the biofilms architecture at micro- and macroscopic scales, driving its complexity and adaptability. Morphologically, this is reflected in mechanical deformations of the biofilm known as wrinkles. In nature, biofilms often host different species of bacteria, allowing for a great diversity of matrix components. Here, we use a combination of two Escherichia coli strains as a model for a multispecies biofilm in which each bacterial strain produces one of two complementary matrix fibres: an amyloid protein (curli) or a polysaccharide (phosphoethanolamine-cellulose). Using fluorescence microscopy, we confirm that the two bacterial strains rapidly segregate into isogenic sectors, decreasing local heterogeneity. Furthermore, we show how wrinkles form, both in the homogenous central region of the biofilm, as well as at the boundary between sectors (i.e. where the two matrix producers co-localize). Finally, we show that increasing strain intermixing via the addition of bacteriophages results in thicker, taller wrinkles, irrespective of whether the two fibres are produced by two different strains or co-produced by the same bacteria.

biophysics↗

bioRxiv2025

Host Physiology Dependent Lysis Timing Shapes Bacteriophage Competition Under Nutrient Fluctuations

When bacteriophages infect starved host bacteria, the restrictive host physiology may lead to prolonged latent periods and/or reduced burst sizes, compared to infection of a fast-growing bacterium. Using a mathematical model, we explore a system of two types of virulent phages that have distinct host physiology dependencies and are infecting a shared bacterial host population. We consider different environmental regimes to test whether they can compete and coexist under fluctuating conditions, putting emphasis on phases with limited resources for bacterial growth. We find that the fitness of a phage that can modulate lysis timing in response to changes in the host physiology is elevated in fluctuating feast-famine environments compared to more stable environments which favor rapid lysis with a reduced burst size. This effect is closely coupled to the increased mortality of free phages due to abortive adsorption to already infected host bacteria during starvation phases. We identify specific system dynamics that either support or suppress the propagation of the delayed lysis phage. This theoretical analysis highlights the competitive benefits and limitations of lysis delay as a phage propagation strategy. Our results underscore the importance of considering the bacterial physiology dependence of bacteriophage replication in order to correctly predict phage fitness and population dynamics in complex environments. IMPORTANCEBacteriophage replication depends strongly on the physiological state of the host, yet most ecological and theoretical studies treat phage life histories as fixed traits. This overlooks how nutrient limitation, starvation, and fluctuating growth conditions reshape infection outcomes. By examining competition between phages with different responses to host physiology, our work shows how environmentally driven changes in the latent period can alter which phages persist, spread, or are lost. These insights clarify when delayed lysis is a beneficial strategy and when it becomes a liability. More broadly, our results highlight the need to integrate host physiology into models of phage-host dynamics to better understand microbial ecosystems and to guide applications such as rational phage therapy design.

microbiology↗