A Markovian Approach towards Bacterial Size Control and Homeostasis in Anomalous Growth Processes

Chen, Yanyan; Baños, Rosa; Buceta, Javier

doi:10.1038/s41598-018-27748-9

Cited by 6 publications

(4 citation statements)

References 42 publications

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“…Finally, the plasticity + eco‐evo model assumes that both supply–demand (plastic) and eco‐evo (rapid evolution) contributions can simultaneously influence the rate of change of M , resulting in the following model for body size dynamics:

\frac{normald M}{normald t} goodbreak= \frac{eK}{N} goodbreak- c M^{δ} goodbreak+ σ^{2} h^{2} \frac{\partial F ()(, M)}{\partial M} .

This model does not account for possible interplay between plastic and evolutionary change, such as plasticity facilitating evolution, plasticity impeding evolution, or evolving plasticity, all of which can occur and have been reviewed elsewhere (Diamond & Martin, 2016). None of our models account for shifts in age or size structure because we were specifically interested in mathematically tracking changes in mean body size, not changes in the entire trait distribution, which require model formulations that are not amenable to ODE fitting (Chen et al, 2018; Nieto‐Acuña et al, 2019).…”

Section: Methodsmentioning

confidence: 99%

Feedbacks between size and density determine rapid eco‐phenotypic dynamics

et al. 2022

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1. Body size is a fundamental trait linked to many ecological processes-from individuals to ecosystems. Although the effects of body size on metabolism are well-known, the potential reciprocal effects of body size and density are less clear. Specifically, (a) whether changes in body size or density more strongly influence the other and (b) whether coupled rapid changes in body size and density are due to plasticity, rapid evolutionary change or a combination of both.2. Here, we address these two issues by experimentally tracking population density and mean body size in the protist Tetrahymena pyriformis as it grows from low density to carrying capacity. We then use Convergent Cross Mapping time series analyses to infer the direction, magnitude and causality of the link between body size and population dynamics. We confirm the results of our analysis by experimentally manipulating body size and density while keeping the other constant. Last, we fit mathematical models to our experimental time series that account for purely plastic change in body size, rapid evolution in size, or a combination of both, to gain insights into the processes that most likely explain the observed dynamics.3. Our results indicate that changes in body size more strongly influence changes in density than the other way around, but also show that there is reciprocity in this effect (i.e., a feedback). We show that a model that only accounts for purely plastic change in size most parsimoniously explains observed, coupled phenotypic and ecological dynamics.4. Together, these results suggest (a) that body size can shift dramatically through plasticity, well within ecological timescales, (b) that rapid changes in body size may have a larger effect on population dynamics than the reverse, but (c) phenotypic and population dynamics influence each other as populations grow.Overall, we show that rapid plastic changes in functional traits like body size may play a fundamental-but currently unrecognized-role in familiar ecological processes such as logistic population growth.

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\frac{normald M}{normald t} goodbreak= \frac{eK}{N} goodbreak- c M^{δ} goodbreak+ σ^{2} h^{2} \frac{\partial F ()(, M)}{\partial M} .

Section: Methodsmentioning

confidence: 99%

Feedbacks between size and density determine rapid eco‐phenotypic dynamics

et al. 2022

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“…None of our models accounts for shifts in age or size structure because here we were are specifically interested in mathematically tracking changes in mean body size, not changes in the entire trait distribution, which also requires model formulations that are not amenable to ODE fitting (Chen, Baños & Buceta 2018; Nieto-Acuña et al . 2019).…”

Section: Methodsmentioning

confidence: 99%

Feedbacks between size and density determine rapid eco-phenotypic dynamics

Gibert

Han

Wieczynski

et al. 2021

Preprint

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1. Body size is a fundamental trait linked to many ecological processes-from individuals to ecosystems. Although the effects of body size on metabolism are well-known, how body size influences, and is influenced by, population growth and density is less clear. Specifically, 1) whether body size, or population dynamics, more strongly influences the other, and, 2) whether observed changes in body size are due to plasticity or rapid evolutionary change, are not well understood. 2. Here, we address these two issues by experimentally tracking population density and mean body size in the protist Tetrahymena pyriformis as it grows from low density to carrying capacity. We then use state-of-the-art time-series analyses to infer the direction, magnitude, and causality of the link between body size and ecological dynamics. Last, we fit two alternative dynamical models to our empirical time series to assess whether plasticity or rapid evolution better explains changes in mean body size. 3. Our results clearly indicate that changes in body size precede and determine changes in population density, not the other way around. We also show that a model assuming that size changes via plasticity more parsimoniously explains these observed coupled phenotypic and ecological dynamics than one that assumes rapid evolution drives changes in size. 4. Together these results suggest that rapid, plastic phenotypic change not only occurs well within ecological timescales but may even precede -and causally influence- ecological dynamics. Furthermore, large individuals may be favored and fuel high population growth rates when population density is low, but smaller individuals may be favored once populations reach carrying capacity and resources become scarcer. Thus, rapid plastic changes in functional traits may play a fundamental and currently unrecognized role in familiar ecological processes like logistic population growth.

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“…Filamentation can also be triggered by exposure to antibiotics (Bos et al, 2015; Chatterjee & Raychaudhuri, 1971; Goormaghtigh & Van Melderen, 2019; Hunt & Pittillo, 1968; Klein & Luginbuhl, 1977; Raghunathan et al, 2020; Ryan & Monsey, 1981; Spratt, 1975) or genetic mutations that specifically inhibit fundamental cell cycle processes, such as DNA replication, cell division or DNA recombination (Allen et al, 1972, 1974; Bi & Lutkenhaus, 1991; Breakefield & Landman, 1973; Ishioka et al, 1998; Lloyd et al, 1988; Mulder & Woldringh, 1989; Rudolph, Upton, Harris, et al, 2009; Rudolph, Upton, & Lloyd, 2009; Van De Putte et al, 1964). Part of these studies reported that filamentation is a reversible morphological change as filaments are generally able to resume division upon return to favorable conditions (Adler & Hardigree, 1965; Barrett et al, 2019; Bos et al, 2015; Chen et al, 2018; Dev Kumar et al, 2019; Goormaghtigh & Van Melderen, 2019; Heinrich et al, 2019; Ishioka et al, 1998; Mulder & Woldringh, 1989; Pribis et al, 2019; Raghunathan et al, 2020; Rudolph et al, 2007; Rudolph, Upton, Harris, et al, 2009; Söderström et al, 2022; Wehrens et al, 2018; Woldringh et al, 1991). Filamentation is even part of the normal life cycle of some bacterial organisms, such as Caulobacter crescentus in freshwater (Allison et al, 1992; Heinrich et al, 2019), the cyanobacterium Synechococcus elongatus growing under dim light (Liao & Rust, 2018) or Legionella pneumophila within biofilms (Piao et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Bacterial filaments recover by successive and accelerated asymmetric divisions that allow rapid post‐stress cell proliferation

Cayron

Dedieu-Berne

Lesterlin

2023

Molecular Microbiology

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Filamentation is a reversible morphological change triggered in response to various stresses that bacteria might encounter in the environment, during host infection or antibiotic treatments. Here we re‐visit the dynamics of filament formation and recovery using a consistent framework based on live‐cells microscopy. We compare the fate of filamentous Escherichia coli induced by cephalexin that inhibits cell division or by UV‐induced DNA‐damage that additionally perturbs chromosome segregation. We show that both filament types recover by successive and accelerated rounds of divisions that preferentially occur at the filaments' tip, thus resulting in the rapid production of multiple daughter cells with tightly regulated size. The DNA content, viability and further division of the daughter cells essentially depends on the coordination between chromosome segregation and division within the mother filament. Septum positioning at the filaments' tip depends on the Min system, while the nucleoid occlusion protein SlmA regulates the timing of division to prevent septum closure on unsegregated chromosomes. Our results not only recapitulate earlier conclusions but provide a higher level of detail regarding filaments division and the fate of the daughter cells. Together with previous reports, this work uncovers how filamentation recovery allows for a rapid cell proliferation after stress treatment.

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A Markovian Approach towards Bacterial Size Control and Homeostasis in Anomalous Growth Processes

Cited by 6 publications

References 42 publications

Feedbacks between size and density determine rapid eco‐phenotypic dynamics

Feedbacks between size and density determine rapid eco‐phenotypic dynamics

Feedbacks between size and density determine rapid eco-phenotypic dynamics

Bacterial filaments recover by successive and accelerated asymmetric divisions that allow rapid post‐stress cell proliferation

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