Mechano-self-regulation of bacterial size in growing colonies

Wittmann, René; Nguyen, G. H. Philipp; Löwen, Hartmut; Sengupta, Anupam; Schwarzendahl, Fabian J.

doi:10.48550/arxiv.2212.10101

Cited by 1 publication

(2 citation statements)

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“…Our insights into the role of nutrient heterogeneity can help to understand how an environment influences the individual reproductive success [63][64][65][66], the spread of neutral mutations [67,68], and the population dynamics in changing environments [69]. To make quantitative predictions, our model can be extended to include processes such as chemotaxis [27][28][29][30][31], density/pressure-dependent growth rates [6,32,33], cell elongation [37,39], polydispersity [70,71], and more complex setup geometries.…”

Section: Discussionmentioning

confidence: 99%

“…The E. coli bacterium, which we have in mind in our model, tends to be less affected by mechanical pressure compared to a variety of epithelial cells [34], so we neglect pressure in this study. However, it should be noted that mechanical self-regulation slows down the elongation rate [37] and in narrow long channels the mechanical forces become the main limiting factor of cell growth [38]. Furthermore, for elongated cells the competition between active and passive forces results in a mosaic of locally ordered patches [39].…”

Section: Introductionmentioning

confidence: 99%

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Dividing active and passive particles in nonuniform nutrient environments

Welker,

Stark

2024

New J. Phys.

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To explore the coupling between a growing population of microorganisms such as E. coli and a nonuniform nutrient distribution, we formulate a minimalistic model. It consists of active Brownian particles that divide and grow at a nutrient-dependent rate following the Monod equation. The nutrient concentration obeys a diffusion equation with a consumption term and a point source. In this setting the heterogeneity in the nutrient distribution can be tuned by the diffusion coefficient. In particle-based simulations, we demonstrate that passive and weakly active particles form proliferation-induced clusters when the nutrient is localized, without relying on further mechanisms such as chemotaxis or adhesion. In contrast, strongly active particles disperse in the whole system during their lifetime and no clustering is present. The steady population is unaffected by activity or nonuniform nutrient distribution and only determined by the ratio of nutrient influx and bacterial death. However, the transient dynamics strongly depends on the nutrient distribution and activity. Passive particles in almost uniform nutrient profiles display a strong population overshoot, with clusters forming all over the system. In contrast, when slowly diffusing nutrients remain centred around the source, the bacterial population quickly approaches the steady state due to its strong coupling to the nutrient. Conversely, the population overshoot of highly active particles becomes stronger when the nutrient localisation increases. We successfully map the transient population dynamics onto a uniform model where the effect of the nonuniform nutrient and bacterial distributions are rationalized by two effective areas.

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