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Karita, Y.

Publications and source records attributed to Karita, Y..

3 recordsLinked to original sources

Context-Dependent Adaptation in Structured Environments

Adaptive evolution often leads to niche specialization, but successful colonization of a new niche can depend as much on ecological context as on genetic change. This is especially true in spatially structured environments, where the physical construction of habitat and the order of arrival of mutants can shape evolutionary outcomes. In static broth cultures, the air-liquid interface (ALI) provides a high-oxygen niche typically colonized by mat-forming mutants. In Pseudomonas fluorescens, a range of single mutations that upregulate cellulose production give rise to "wrinkly spreader" (WS) types--canonical niche specialists that out-compete ancestral types at the ALI. Yet we discover that this is a half-truth: WS mutants frequently fail to establish when introduced alone at low density, but co-culture with ancestral types rescues colonization. Microscopy and model simulations show that ancestors physically scaffold the ALI, enabling stable attachment and facilitating the in situ emergence of an array of genetically diverse WS mutants. Ancestors later disperse, vacate the niche allowing WS mutant expansion. This transient asymmetric interaction reveals that even strongly adaptive mutations may require ecological facilitation to succeed. More broadly, our findings challenge simple narratives of adaptive replacement and underscore how transient ecological dependencies can shape the trajectory of evolutionary change.

evolutionary biology↗

Scale-dependent tipping points of bacterial colonization resistance

Bacteria are efficient colonizers of a wide range of secluded micro-habitats, such as soil pores, skin follicles, or intestinal crypts. How the structural diversity of these habitats modulates microbial self-organization remains poorly understood, in part because of the challenge to specifically manipulate the physical structure of microbial environments. Using a microfluidic device to grow bacteria in crypt-like incubation chambers of systematically varied lengths, we show that small variations in the physical structure of the micro-habitat can drastically alter bacterial colonization success and resistance against invaders. Small crypts are un-colonizable, intermediately sized crypts can stably support dilute populations, while beyond a second critical lengthscale, populations phase-separate into a dilute and a jammed region. The jammed state is characterized by extreme colonization resistance, even if the resident strain is suppressed by an antibiotic. Combined with a flexible biophysical model, we demonstrate that colonization resistance and associated priority effects can be explained by a crowding-induced phase transition, which results from a competition between proliferation and density-dependent cell leakage. The emerging sensitivity to scale underscores the need to control for scale in microbial ecology experiments. Systematic flow-adjustable lengthscale variations may serve as a promising strategy to elucidate further scale-sensitive tipping points and to rationally modulate the stability and resilience of microbial colonizers.

ecology↗

Impact of crowding on the diversity of expanding populations

Crowding effects are key to the self-organization of densely packed cellular assemblies, such as biofilms, solid tumors, and developing tissues. When cells grow and divide they push each other apart, remodeling the structure and extent of the populations range. It has recently been shown that crowding has a strong impact on the strength of natural selection. However, the impact of crowding on neutral processes remains unclear, which controls the fate of new variants as long as they are rare. Here, we quantify the genetic diversity of expanding microbial colonies and uncover signatures of crowding in the site frequency spectrum. By combining Luria-Delbruck fluctuation tests, lineage tracing in a novel microfluidic incubator, cell-based simulations, and theoretical modeling, we find that the majority of mutations arise behind the expanding frontier, giving rise to clones that are mechanically "pushed out" of the growing region by the proliferating cells in front. These excluded-volume interactions result in a clone size distribution that solely depends on where the mutation first arose relative to the front and is characterized by a simple power-law for low-frequency clones. Our model predicts that the distribution only depends on a single parameter, the characteristic growth layer thickness, and hence allows estimation of the mutation rate in a variety of crowded cellular populations. Combined with previous studies on high-frequency mutations, our finding provides a unified picture of the genetic diversity in expanding populations over the whole frequency range and suggests a practical method to assess growth dynamics by sequencing populations across spatial scales. Significance StatementGrowing cell populations become densely packed as cells proliferate and fill space. Crowding prevents spatial mixing of individuals, significantly altering the evolutionary outcome from established results for well-mixed populations. Despite the fundamental differences between spatial and well-mixed populations, little is known about the impact of crowding on genetic diversity. Looking at microbial colonies growing on plates, we show that the allele frequency spectrum is characterized by a simple power law for low frequencies. Using cell-based simulations and microfluidic experiments, we identify the origin of this distribution in the volume-exclusion interactions within the crowded cellular environment, enabling us to extend this findings to a broad range of densely packed populations. This study highlights the importance of cellular crowding for the emergence of rare genetic variants.

biophysics↗