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Stocker, R.

Publications and source records attributed to Stocker, R..

At least 37 records · Page 2Linked to original sources

Mechanism of bacterial predation via ixotrophy

Predation allows bacteria to access alternative substrates in low-nutrient conditions. Ixotrophy has been proposed as a predatory lifestyle of multicellular filamentous bacteria in aquatic environments; however, the molecular mechanism remains unknown. Here we uncover by a multidisciplinary approach that ixotrophy requires the interplay of multiple cellular machineries and a regulatory mechanism. Attacker-prey contacts are established by gliding motility and extracellular grappling hook-like structures that bind prey flagella. Cryo-electron microscopy identifies the grappling hooks as a heptameric assembly of a Type 9 Secretion System substrate. Cryo-electron tomography and functional assays show that killing is mediated by puncturing of the prey cell using a Type 6 Secretion System, possibly triggered by extracellular antennae. Single-cell analyses with stable isotope-labeled prey demonstrate that prey components are taken up by the attacker. Depending on nutrient availability, ixotrophy is switched off by endogenous Insertion Sequence Elements and re-activated through their excision. A marine metagenomic time series provides evidence for coupled dynamics of ixotrophic bacteria and their prey. Our study reveals the complex mechanism of a conserved microbial predatory lifestyle and indicates the need for its regulation in conditions where the expression of costly pathways is dispensable.

microbiology↗

Variability in single-cell oxygen consumption kinetics

We combined microfabricated devices with multiparameter identification algorithms to probe the variability in size-dependent oxygen consumption parameters of single human hepatic cells. We demonstrate that single cells exhibit an oxygen-dependent metabolic rate, typical of Michaelis-Menten kinetics, and that their maximal oxygen consumption is significantly lower than that of monolayers or 3D hepatic cell aggregates. Notably, we found that clusters of two or more cells competing for a limited oxygen supply reduced their maximal single-cell consumption rate, highlighting their ability to adapt to local resource availability and the presence of nearby cells. Next, we used our high-throughput approach to characterize the covariance of size and oxygen consumption within a cell population. The results show that cooperative behaviour emerges in cell clusters, and that single-cell size and metabolism can be described by a lognormal joint probability density. Our study thus serves as a foundation to connect the metabolic activity of single human hepatocytes to their tissue-or organ-level metabolism as well as describe its size-related variability through scaling laws.

bioengineering↗

Microbial metabolic specificity controls pelagic lipid export efficiency

Lipids comprise more than 20% of sinking organic matter in the ocean and play a crucial role in the carbon cycle. Despite this, our understanding of the processes that control lipid degradation is limited. Here we combined nano-lipidomics and imaging to study the bacterial degradation of diverse algal lipid droplets. Bacteria isolated from natural marine particles exhibited distinct dietary preferences, ranging from selective to promiscuous degraders. Dietary preference was associated with a distinct set of lipid degradation genes rather than with taxonomic origin. The top degrader, Pseudomonas zhaodongensis, rapidly consumed triacylglycerols (TAGs) from lipid extracts while promoting colonization of kin by chemotaxis toward glycerol, the TAG degradation product. Using synthetic communities composed of isolates with distinct dietary preferences, we demonstrated that lipid degradation is modulated by microbial interactions. A particle export model incorporating these dynamics suggests that metabolic specialization and community dynamics influences lipid transport efficiency in the oceans mesopelagic zone.

ecology↗

Myeloperoxidase activity predicts atherosclerotic plaque disruption and atherothrombosis

BackgroundUnstable atherosclerotic plaque is characterized by increased myeloperoxidase (MPO) activity. As unstable plaque is vulnerable to disruption and ensuing thrombosis, we examined whether plaque MPO activity predicts atherothrombosis in a pre-clinical model and correlates with ruptured human atheroma. MethodsTo assess if plaque MPO activity predicts atherothrombosis, rabbits were subjected to aortic endothelial denudation, cholesterol feeding, in vivo magnetic resonance imaging (MRI) of MPO activity using MPO-Gd (gadolinium), followed by pharmacological triggering of atherothrombosis, histology, and MPO activity determined by liquid chromatography tandem mass spectrometry (LC-MSMS) by quantifying the MPO-specific product of hydroethidine, 2-chloroethidium. To correlate plaque MPO activity to ruptured human atheroma, ex vivo determination of MPO activity by MPO-Gd retention in carotid endarterectomy (CEA) specimens was correlated with in vivo MRI plaque phenotyping in patients, histology, and MPO activity determined by LC-MSMS. ResultsIn rabbits, pre-trigger in vivo MPO activity, validated by LC-MSMS and histology, was higher in thrombosis-prone than thrombosis-resistant plaques and lesion-free segments (R1 relaxation rate = 2.2 {+/-} 0.4 versus 1.6 {+/-} 0.2 and 1.5 {+/-} 0.2 s-1, respectively, p<0.0001), and it predicted atherothrombosis. In CEA specimens, MPO-Gd retention was greater in histologic and MRI-graded American Heart Association (AHA) type VI than types III, IV and V plaques ({Delta}R1 relaxation rate from baseline = 48 {+/-} 6 versus 16 {+/-} 7, 17 {+/-} 8 and 23 {+/-} 8%, respectively, p<0.0001). This association was confirmed by comparing AHA grade to MPO activity determined by LC-MSMS (277 {+/-} 338 versus 7 {+/-} 6, 11 {+/-} 12 and 42 {+/-} 39 pmol 2-chloroethidium/mg protein for type VI versus type III-V plaques, respectively, p=0.0008). ConclusionsMPO activity is elevated in thrombosis-prone rabbit and ruptured human atheroma. Non-invasive molecular imaging of MPO activity predicts atherothrombosis, highlighting the potential of arterial MPO activity to detect vulnerable, destabilized atherosclerosis.

biochemistry↗

Colchicine promotes atherosclerotic plaque stability independently of inflammation

Atherosclerosis is a chronic inflammatory disease which is driven in part by the aberrant trans-differentiation of vascular smooth muscle cells (SMCs). No therapeutic drug has been shown to reverse detrimental SMC-derived cell phenotypes into protective phenotypes, a hypothesized enabler of plaque regression and improved patient outcome. Herein, we describe a novel function of colchicine in the beneficial modulation of SMC-derived cell phenotype, independent of its conventional anti-inflammatory effects. Using SMC fate mapping in an advanced atherosclerotic lesion model, colchicine induced plaque regression by converting pathogenic SMC-derived macrophage-like and osteoblast-like cells into protective myofibroblast-like cells which thickened, and thereby stabilized, the fibrous cap. This was dependent on Notch3 signaling in SMC-derived plaque cells. These findings may help explain the success of colchicine in clinical trials relative to other anti-inflammatory drugs. Thus, we demonstrate the potential of regulating SMC phenotype in advanced plaque regression through Notch3 signaling, in addition to the canonical anti-inflammatory actions of drugs to treat atherosclerosis.

cell biology↗

Polysaccharide breakdown products drive degradation-dispersal cycles of foraging bacteria through changes in metabolism and motility

Most of Earths biomass is composed of polysaccharides. During biomass decomposition, polysaccharides are degraded by heterotrophic bacteria as a nutrient and energy source and are thereby partly remineralized into CO2. As polysaccharides are heterogeneously distributed in nature, following the colonization and degradation of a polysaccharide hotspot the cells need to reach new polysaccharide hotspots. Even though many studies indicate that these degradation-dispersal cycles contribute to the carbon flow in marine systems, we know little about how cells alternate between polysaccharide degradation and motility, and which environmental factors trigger this behavioral switch. Here, we studied the growth of the marine bacterium Vibrio cyclitrophicus ZF270 on the abundant marine polysaccharide alginate, both in its soluble polymeric form as well as on its breakdown products. We used microfluidics coupled to time-lapse microscopy to analyze motility and growth of individual cells, and RNA sequencing to study associated changes in gene expression. We found that single cells grow at reduced rate on alginate until they form large groups that cooperatively break down the polymer. Exposing cell groups to digested alginate accelerates cell growth and changes the expression of genes involved in alginate degradation and catabolism, central metabolism, ribosomal biosynthesis, and transport. However, exposure to digested alginate also triggers cells to become motile and disperse from cell groups, proportionally increasing with the group size before the nutrient switch, and this is accompanied by high expression of genes involved in flagellar assembly, chemotaxis, and quorum sensing. The motile cells chemotax toward polymeric but not digested alginate, likely enabling them to find new polysaccharide hotspots. Overall, our findings reveal cellular mechanisms that might also underlie bacterial degradation-dispersal cycles, which influence the remineralization of biomass in marine environments. ImportancePolysaccharides, also known as glycans, are the most abundant form of biomass on Earth and understanding how they are degraded by microorganisms is essential for our understanding of the global carbon cycle and the storage and release of CO2 by natural systems. Although group formation is a common strategy used by bacterial cells to degrade ubiquitous polymeric growth substrates in nature, where nutrient hotspots are heterogeneously distributed, little is known about how cells prepare for dispersal from an exhausted nutrient source and re-initiate degradation of new nutrient patches. By quantifying growth, motility and chemotaxis of individual cells and comparing gene expression changes when populations were exposed to either polysaccharides or their degradation products in the form of digested polysaccharides, we show that bacterial cells alter their behavior when they experience a shift from polymeric to digested polysaccharides: After cells form groups during growth on polymers, the exposure to degradation products triggered cells to become motile, enabling dispersal from sessile cell groups. The chemotactic attraction of motile cells to polymeric alginate likely allows cells to move towards new polysaccharide hotspots. Our study sheds light on the cellular processes that drive bacterial growth and behavior during carbon remineralization, an important process resulting in CO2 release from natural systems.

microbiology↗

Interspecies interactions determine growth dynamics of biopolymer degrading populations in microbial communities.

Microbial communities perform essential ecosystem functions such as the remineralization of organic carbon that exists as biopolymers. The first step in mineralization is performed by biopolymer degraders, which harbor enzymes that can break down polymers into constituent oligo- or monomeric forms. The released nutrients not only allow degraders to grow, but also promote growth of cells that either consume the breakdown products, i.e., exploiters, or consume metabolites released by the degraders, i.e., scavengers. It is currently not clear how such remineralizing communities assemble at the microscale - how interactions between the different guilds influence their growth and spatial distribution, and hence the development and dynamics of the community. Here we address this knowledge gap by studying marine microbial communities that grow on the abundant marine biopolymer alginate. We used batch growth assays and microfluidics coupled to time-lapse microscopy to quantitatively investigate growth and spatial distribution of single cells. We found that the presence of exploiters or scavengers alters the spatial distribution of degrader cells. In general, exploiters and scavengers - which we collectively refer to as consumer cells - slowed down the growth of degrader cells. In addition, coexistence with consumers altered the production of the extracellular enzymes that breakdown polymers by degrader cells. Our findings reveal that ecological interactions by non-degrading community members have a profound impact on the functions of microbial communities that remineralize carbon biopolymers in nature. ImportanceBiopolymers are the most abundant source of carbon on the planet and their breakdown by microbial degraders releases metabolic products that allow cross-feeding cells to grow and fuel the assembly of microbial communities. While it is known that the growth of degraders can facilitate growth of downstream cross-feeders in microbial communities, it has remained generally unclear if and how cross-feeders influence growth of degraders. Bridging this knowledge gap is important because degraders primarily drive the remineralization of carbon, a central process in the carbon cycle. We found that the presence cross-feeders can influence the growth of degraders by altering their spatial distribution as well as extracellular breakdown enzyme activity. Our study sheds light on the role of microbial interactions in shaping the rate of carbon remineralization in nature.

microbiology↗

Intercellular collectivity is governed by enzyme secretion strategies in marine polysaccharide degrading bacteria

Polysaccharide breakdown by bacteria requires the activity of enzymes that degrade polymers extracellularly. This generates a localized pool of breakdown products that are accessible to the enzyme producers themselves as well as to other organisms. Marine bacterial taxa often show marked differences in the production and secretion of degradative enzymes that break down polysaccharides. These differences can have profound effects on the pool of diffusible breakdown products and hence on the ecological dynamics. However, the consequences of differences in enzymatic secretions on cellular growth dynamics and interactions are unclear. Here we combine experiments and models to study the growth dynamics of single cells within populations of marine Vibrionaceae strains that grow on the abundant marine polymer alginate, using microfluidics coupled to quantitative single-cell analysis and mathematical modelling. We find that strains that have low extracellular secretions of alginate lyases show stronger aggregative behaviors compared to strains that secrete high levels of enzymes. One plausible reason for this observation is that low secretors require a higher cellular density to achieve maximal growth rates in comparison with high secretors. Our findings indicate that increased aggregation increases intercellular synergy amongst cells of low-secreting strains. By mathematically modelling the impact of the level of degradative enzyme secretion on the rate of oligomer loss to diffusion, we find that enzymatic capability modulates the propensity of cells within clonal populations to cooperate or compete with each other. Our experiments and models demonstrate that marine bacteria display distinct aggregative behaviors and intercellular interactions based on their enzymatic secretion capabilities when growing on polysaccharides.

microbiology↗

A microfluidic platform for characterizing the structure and rheology of biofilm streamers

Biofilm formation is the most successful survival strategy for bacterial communities. In the biofilm lifestyle, bacteria embed themselves in a self-secreted matrix of extracellular polymeric substances (EPS), which acts as a shield against mechanical and chemical insults. When ambient flow is present, this viscoelastic scaffold can take a streamlined shape, forming biofilm filaments suspended in flow, called streamers. Streamers significantly disrupt the fluid flow by causing rapid clogging and affect transport in aquatic environments. Despite their relevance, the structural and rheological characterization of biofilm streamers is still at an early stage. In this work, we present a microfluidic platform that allows the reproducible growth of biofilm streamers in controlled physico-chemical conditions and the characterization of their biochemical composition, morphology, and rheology in situ. We employed isolated micropillars as nucleation sites for the growth of single biofilm streamers under the continuous flow of a diluted bacterial suspension. By combining fluorescent staining of the EPS components and epifluorescence microscopy, we were able to characterize the biochemical composition and morphology of the streamers. Additionally, we optimized a protocol to perform hydrodynamic stress tests in situ, by inducing controlled variations of the fluid shear stress exerted on the streamers by the flow. Thus, the reproducibility of the formation process and the testing protocol make it possible to perform several consistent experimental replicates that provide statistically significant information. By allowing the systematic investigation of the role of biochemical composition on the structure and rheology of streamers, this platform will advance our understanding of biofilm formation.

biophysics↗

Bacterial chemotaxis to saccharides is governed by a trade-off between sensing and uptake

To swim up gradients of nutrients, E. coli senses nutrient concentrations within its periplasm. For small nutrient molecules, periplasmic concentrations typically match extracellular concentrations. However, this is not necessarily the case for saccharides, such as maltose, which is transported into the periplasm via a specific porin. Previous observations have shown that under various conditions E. coli limits maltoporin abundance so that, for extracellular micromolar concentrations of maltose, there are predicted to be only nanomolar concentrations of free maltose in the periplasm. Thus, in the micromolar regime, the total uptake of maltose from the external environment into the cytoplasm is limited not by the abundance of cytoplasmic transport proteins but by the abundance of maltoporins. Here we present results from experiments and modeling showing that this porin-limited transport enables E. coli to sense micromolar gradients of maltose despite having a high-affinity ABC transport system that is saturated at these micromolar levels. We used microfluidic assays to study chemotaxis of E. coli in various gradients of maltose and methyl-aspartate and leveraged our experimental observations to develop a mechanistic transport-and-sensing chemotaxis model. Incorporating this model into agent-based simulations, we discover a trade-off between uptake and sensing: although high-affinity transport enables higher uptake rates at low nutrient concentrations, it severely limits dynamic sensing range. We thus propose that E. coli may limit periplasmic uptake to increase its chemotactic sensitivity, enabling it to use maltose as an environmental cue. Statement of SignificanceBacterial chemotaxis is among the best-studied systems in biology and is paradigmatic of the mechanisms used by cells to link sensory inputs with regulated responses, thus providing insight into the ecological basis of cellular physiology. Here we present a mechanistic chemotaxis model that describes how the regulation of the transport of a sugar into and out of the cells periplasm affects the cells motile response to that sugar. Based on observations from population-level chemotaxis assays, we uncover an ecologically relevant trade-off between sensing and uptake. The general finding of this work is that, while high-affinity transport allows for higher uptake rates, it can severely limit the cells dynamic sensing range.

microbiology↗

The structural role of bacterial eDNA in the formation of biofilm streamers

Across diverse habitats, bacteria are mainly found as biofilms, surface-attached communities embedded in a self-secreted matrix of extracellular polymeric substances (EPS), which enhances bacterial resistance to antimicrobial treatment and mechanical stresses. In the presence of flow and geometric constraints such as corners or constrictions, biofilms take the form of long, suspended threads known as streamers, which bear important consequences in industrial and clinical settings by causing clogging and fouling. The formation of streamers is thought to be driven by the viscoelastic nature of the biofilm matrix. Yet, little is known about the structural composition of streamers and how it affects their mechanical properties. Here, using a microfluidic platform that allows growing and precisely examining biofilm streamers, we show that extracellular DNA (eDNA) constitutes the backbone and is essential for the mechanical stability of Pseudomonas aeruginosa s streamers. This finding is supported by the observations that DNA-degrading enzymes prevent the formation of streamers and clear already formed ones, and that the antibiotic ciprofloxacin promotes their formation by increasing the release of eDNA. Furthermore, using mutants for production of the exopolysaccharide Pel, an important component of P. aeruginosa s EPS, we reveal a new, although indirect role of Pel, in tuning the mechanical properties of the streamers. Taken together, these results highlight the importance of eDNA and of its interplay with Pel in determining the mechanical properties of P. aeruginosa streamers, and suggest that targeting the composition of streamers can be an effective approach to control the formation of these biofilm structures.

biophysics↗

Heme oxygenase limits mycobacterial infection-induced ferroptosis

Iron homeostasis is essential for both sides of the host-pathogen interface. Restricting access of iron slows bacterial growth while iron is also a necessary co-factor for host immunity. Heme oxygenase 1 (HMOX1) is a critical regulator of iron homeostasis that catalyses the liberation of iron during degradation of heme. It is also a stress-responsive protein that can be rapidly upregulated and confers protection to the host. Although a protective role of HMOX1 has been demonstrated in a variety of diseases, the role of HMOX1 in Mycobacterium tuberculosis infection is equivocal across experiments with different host-pathogen combinations. Here we use the natural host-pathogen pairing of the zebrafish-Mycobacterium marinum infection platform to study the role of zebrafish heme oxygenase in mycobacterial infection. We identify zebrafish Hmox1a as the relevant functional paralog of mammalian HMOX1 and demonstrate a conserved role for Hmox1a in protecting the host from mycobacterial infection. Using genetic and chemical tools, we show zebrafish Hmox1a protects the host against mycobacterial infection by reducing infection-induced iron accumulation and ferroptosis.

immunology↗

Zebrafish heme oxygenase 1a is necessary for normal development and macrophage migration

Heme oxygenase function is highly conserved between vertebrates where it plays important roles in normal embryonic development and controls oxidative stress. Expression of the zebrafish heme oxygenase 1 genes are known to be responsive to oxidative stress suggesting a conserved physiological function. Here we generate a knockout allele of zebrafish hmox1a and characterize the effects of hmox1a and hmox1b loss on embryonic development. We find that loss of hmox1a or hmox1b causes developmental defects in only a minority of embryos, in contrast to Hmox1 gene deletions in mice that causes loss of most embryos. Using a tail wound inflammation assay we find a conserved role for hmox1a, but not hmox1b, in normal macrophage migration to the wound site. Together our results indicate zebrafish hmox1a has clearly a partitioned role from hmox1b that is more consistent with conserved functions of mammalian Heme oxygenase 1.

developmental biology↗

Mechanistic model of nutrient uptake explains dichotomy between marine oligotrophic and copiotrophic bacteria

Marine heterotrophic bacteria use a spectrum of nutrient uptake strategies, from that of copiotrophs--which dominate in nutrient-rich environments--to that of oligotrophs--which dominate in nutrient-poor environments. While copiotrophs possess numerous phosphotransferase systems (PTS), oligotrophs lack PTS and rely on ATP-binding cassette (ABC) transporters, which use binding proteins. Here we present a molecular-level model that explains the dichotomy between oligotrophs and copiotrophs as the consequence of trade-offs between PTS and ABC transport. When we approximate ABC transport in Michaelis-Menten form, we find, contrary to the canonical formulation, that its half-saturation concentration KM is not a constant but instead a function of binding protein abundance. Thus, oligotrophs can attain nanomolar KM values using binding proteins with micromolar dissociation constants and while closely matching transport and metabolic capacities. However, this requires large periplasms and high abundances of binding proteins, whose slow diffusion limits uptake rate. We conclude that the use of binding proteins is critical for oligotrophic survival yet severely constrains maximal growth rates, thus fundamentally shaping the divergent evolution of oligotrophs and copiotrophs.

microbiology↗

A distinct growth physiology enhances bacterial growth under rapid nutrient fluctuations

It has been long known that bacteria coordinate their physiology with environmental nutrient, yet our current understanding offers little intuition for how bacteria respond to the second-to-minute scale fluctuations in nutrient concentration characteristic of many microbial habitats. To investigate the effects of rapid nutrient fluctuations on bacterial growth, we coupled custom microfluidics with single-cell microscopy to quantify the growth rate of E. coli experiencing 30 s to 60 min nutrient fluctuations. Compared to steady environments of equal average concentration, fluctuating environments reduced growth rate by up to 50%. However, measured reductions in growth rate were only 38% of the growth loss predicted from single nutrient shifts -- an enhancement produced by the distinct growth response of cells grown in environments that fluctuate rather than shift once. We report an unexpected physiology adapted for growth in nutrient fluctuations and implicate nutrient timescale as a critical environmental parameter beyond nutrient concentration and source.

microbiology↗

Bistability in oxidative stress response determines the migration behavior of phytoplankton in turbulence

Turbulence is an important determinant of phytoplankton physiology, often leading to cell stress and damage. Turbulence affects phytoplankton migration, both by transporting cells and by triggering switches in migratory behavior, whereby vertically migrating cells can invert their direction of migration upon exposure to turbulent cues. However, a mechanistic link between single-cell physiology and vertical migration of phytoplankton in turbulence is currently missing. Here, by combining physiological and behavioral experiments with a mathematical model of stress accumulation and dissipation, we show that the mechanism responsible for the switch in the direction of migration in the marine raphidophyte Heterosigma akashiwo is the integration of reactive oxygen species (ROS) signaling generated by turbulent cues. Within timescales as short as tens of seconds, the emergent downward-migrating subpopulation exhibited a two-fold increase of ROS, an indicator of stress, 15% lower photosynthetic efficiency, and 35% lower growth rate over multiple generations compared to the upward-migrating subpopulation. The origin of the behavioral split in a bistable oxidative stress response is corroborated by the observation that exposure of cells to exogenous stressors (H2O2, UV-A radiation or high irradiance), in lieu of turbulence, caused comparable ROS accumulation and an equivalent split into the two subpopulations. By providing a mechanistic link between single-cell physiology, population-scale migration and fitness, these results contribute to our understanding of phytoplankton community composition in future ocean conditions. Significance StatementTurbulence has long been known to drive phytoplankton fitness and species succession: motile species dominate in calmer environments and non-motile species in turbulent conditions. Yet, a mechanistic understanding of the effect of turbulence on phytoplankton migratory behavior and physiology is lacking. By combining a method to generate turbulent cues, quantification of stress accumulation and physiology, and a mathematical model of stress dynamics, we show that motile phytoplankton use their mechanical stability to sense the intensity of turbulent cues and integrate these cues in time via stress signaling to trigger switches in migratory behavior. The stress-mediated warning strategy we discovered provides a paradigm for how phytoplankton cope with turbulence, thereby potentially governing which species will be successful in a changing ocean.

biophysics↗

The effect of flow on swimming bacteria controls the initial colonization of curved surfaces

The colonization of solid surfaces by bacteria is a widespread phenomenon with major consequences on environmental processes, biotechnology and human health. While much is known about the molecular mechanisms of surface colonization, the influence of the physical environment remains poorly understood. Here we show that the magnitude and location of colonization of non-planar surfaces by motile bacteria is largely controlled by the local flow conditions. Using microfluidic experiments with Pseudomonas aeruginosa and Escherichia coli, we demonstrate that the velocity gradients created by a curved surface drive preferential attachment to specific regions of the collecting surface, namely the leeward side of cylinders and immediately downstream of apexes on corrugated surfaces, locations that are in stark contrast to where non-motile cells attach. The preferential attachment location depends on the local hydrodynamic conditions and, as revealed by a mathematical model benchmarked on the observations, on cell morphology and swimming traits, while it is independent of the physicochemical properties of the surface. The interplay between imposed flow and bacterial motility further affects the overall attachment rate, increasing it by up to two orders of magnitude compared to the non-motile case at moderate flow velocities of up to twenty times the bacterial swimming speed. These results highlight the importance of fluid flow on the magnitude and location of bacterial colonization of surfaces and provide a mechanistic model to predict colonization in flow for a wide range of applications, from infection biology to bioremediation and biofouling.

biophysics↗

Bacterial glycogen provides short-term benefits in changing environments

Changing nutritional conditions challenge microbes and shape their evolutionary optimization. Here we investigated the role of glycogen in dynamic physiological adaptation of Escherichia coli to fluctuating nutrients following carbon starvation using real-time metabolomics. We found significant metabolic activity remaining after the depletion of environmental glucose that was linked to a rapid utilization of intracellular glycogen. Glycogen was depleted by 80% within minutes of glucose starvation and similarly replenished within minutes of glucose availability. These fast timescales of glycogen utilization correspond to the short-term benefits that glycogen provided to cells undergoing various physiological transitions. Cells capable of utilizing glycogen exhibited shorter lag times than glycogen mutants when starved between different carbon sources. The ability to utilize glycogen was also important for the transition between planktonic and biofilm lifestyles and enabled increased glucose uptake during pulses of limited glucose availability. While wild-type and mutant strains exhibited comparable growth rates in steady environments, mutants deficient in glycogen utilization grew more poorly in environments that fluctuated on minute-scales between carbon availability and starvation. Altogether, these results highlight an underappreciated role of glycogen to rapidly provide carbon and energy in changing environments, thereby increasing survival and competition capabilities in fluctuating and nutrient poor conditions.

microbiology↗