Optimal dormancy strategies in fluctuating environments given delays in phenotypic switching

Măgălie, Andreea; Schwartz, Daniel; Lennon, Jay T.; Weitz, Joshua S.

doi:10.1016/j.jtbi.2023.111413

Cited by 4 publications

(5 citation statements)

References 24 publications

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“…We next evaluated the robustness of our findings for Model V by including a more realistic delay before the onset of dormancy, through the introduction of a sequence of multiple intermittent states n E (see Methods, Model V). Given the inclusion of a delay before dormant cells resist subsequent viral infection [53], we find that Model V continues to reproduce plaque growth dynamics (see Fig. 5C and Fig.…”

Section: Resultsmentioning

confidence: 94%

“…Model R assumes that sporulation in Bacillus subtillis is triggered by starvation [3, 43, 51], specifically, dormancy is initiated at a low rate when resources are high and at a much higher rate when resources are depleted [52, 53]. The associated partial differential equations are as follows: Where is the rescaled density of resources, expressed in units of cells/mL.…”

Section: Methodsmentioning

confidence: 99%

“…In Model V, dormancy can be initiated via starvation or with a probability p ∈ (0, 1) upon interacting with a virus particle. This yields a family of ( p, σ ) combinations that exhibit identical plaque growth dynamics, with the ( p = 0, ) case corresponding to Model R. In order to account for a time delay for spore formation we introduce a series of multiple sequential stages n E to become dormant [53]. Hence, the dormancy initiation time follows an Erlang distribution.…”

Section: Methodsmentioning

confidence: 99%

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Phage infection fronts trigger early sporulation and collective defense in bacterial populations

Măgălie,

Marantos,

Schwartz

et al. 2024

Preprint

Self Cite

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I.ABSTRACTBacteriophage (phage) infect, lyse, and propagate within bacterial populations. However, physiological changes in bacterial cell state can protect against infection even within genetically susceptible populations. One such example is the generation of endospores byBacillusand its relatives, characterized by a reversible state of reduced metabolic activity that protects cells against stressors including desiccation, energy limitation, antibiotics, and infection by phage. Here we tested how sporulation at the cellular scale impacts phage dynamics at population scales when propagating amongstB. subtilisin spatially structured environments. Initially, we found that plaques resulting from infection and lysis were approximately 3-fold smaller on lawns of sporulating wild-type bacteria vs. non-sporulating bacteria. Notably, plaque size was reduced due to an early termination of expanding phage plaques rather than the reduction of plaque growth speed. Microscopic imaging of the plaques revealed ‘sporulation rings’, i.e., spores enriched around plaque edges relative to phage-free regions. We developed a series of mathematical models of phage, bacteria, spore, and small molecules that recapitulate plaque dynamics and identify a putative mechanism: sporulation rings arise in response to lytic activity. In aggregate, sporulation rings inhibit phage from accessing susceptible cells even when sufficient resources are available for further infection and lysis. Together, our findings identify how dormancy can self-limit phage infections at population scales, opening new avenues to explore the entangled fates of phages and their bacterial hosts in environmental and therapeutic contexts.

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Section: Resultsmentioning

confidence: 94%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Phage infection fronts trigger early sporulation and collective defense in bacterial populations

Măgălie,

Marantos,

Schwartz

et al. 2024

Preprint

Self Cite

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“…In the metastatic niche, DTCs form a metastasis or enter in the dormant period, when cancer cells exit the cell cycle, arrest their growth, and become immune to drugs that usually target cells in mitotic division [284]. Dormancy is known as a reversible state of reduced metabolic activity, known as a dynamic mechanism by which the organisms/cells respond to periods of unfavorable environmental/microenvironmental stress, including temperature, low nutrients, or toxins [285]. For example, the bone is considered a particularly hypoxic environment, where the oxygen levels range from <1% to 6% (approximately 7-43 mm Hg), compared with most normal tissues, where oxygen levels ranges between 2% and 9% (14-65 mm Hg) [286].…”

Section: Breast Tumor As a Macrosystemmentioning

confidence: 99%

Onco-Breastomics: An Eco-Evo-Devo Holistic Approach

Neagu,

Whitham,

Bruno

et al. 2024

IJMS

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Known as a diverse collection of neoplastic diseases, breast cancer (BC) can be hyperbolically characterized as a dynamic pseudo-organ, a living organism able to build a complex, open, hierarchically organized, self-sustainable, and self-renewable tumor system, a population, a species, a local community, a biocenosis, or an evolving dynamical ecosystem (i.e., immune or metabolic ecosystem) that emphasizes both developmental continuity and spatio-temporal change. Moreover, a cancer cell community, also known as an oncobiota, has been described as non-sexually reproducing species, as well as a migratory or invasive species that expresses intelligent behavior, or an endangered or parasite species that fights to survive, to optimize its features inside the host’s ecosystem, or that is able to exploit or to disrupt its host circadian cycle for improving the own proliferation and spreading. BC tumorigenesis has also been compared with the early embryo and placenta development that may suggest new strategies for research and therapy. Furthermore, BC has also been characterized as an environmental disease or as an ecological disorder. Many mechanisms of cancer progression have been explained by principles of ecology, developmental biology, and evolutionary paradigms. Many authors have discussed ecological, developmental, and evolutionary strategies for more successful anti-cancer therapies, or for understanding the ecological, developmental, and evolutionary bases of BC exploitable vulnerabilities. Herein, we used the integrated framework of three well known ecological theories: the Bronfenbrenner’s theory of human development, the Vannote’s River Continuum Concept (RCC), and the Ecological Evolutionary Developmental Biology (Eco-Evo-Devo) theory, to explain and understand several eco-evo-devo-based principles that govern BC progression. Multi-omics fields, taken together as onco-breastomics, offer better opportunities to integrate, analyze, and interpret large amounts of complex heterogeneous data, such as various and big-omics data obtained by multiple investigative modalities, for understanding the eco-evo-devo-based principles that drive BC progression and treatment. These integrative eco-evo-devo theories can help clinicians better diagnose and treat BC, for example, by using non-invasive biomarkers in liquid-biopsies that have emerged from integrated omics-based data that accurately reflect the biomolecular landscape of the primary tumor in order to avoid mutilating preventive surgery, like bilateral mastectomy. From the perspective of preventive, personalized, and participatory medicine, these hypotheses may help patients to think about this disease as a process governed by natural rules, to understand the possible causes of the disease, and to gain control on their own health.

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“…Such a strategy is employed for instance by cells to cope with antibiotics [11], by phages to optimize their infection strategy of bacteria [12], or by plants to cope with a fluctuating climate [13, 14]. All these three examples involve a dormant state which protects individuals from harsh conditions in the environment, while preserving the biodiversity in a seed bank [15].…”

Section: Introductionmentioning

confidence: 99%

The trade-off between growth and risk in Kelly’s gambling and beyond

Cavallero,

Rousselot,

Pugatch

et al. 2023

Preprint

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We study a generalization of Kelly’s horse model to situations where gambling on horses other than the winning horse does not lead to a complete loss of the investment. In such a case, the odds matrix is non-diagonal, a case which is of special interest for biological applications. We derive a trade-off for this model between the mean growth rate and the volatility as a proxy for risk. We show that this trade-off is related to a game-theoretic formulation of this problem developed previously. Since the effect of fluctuations around the average growth rate is asymmetric, we also study how the risk-growth trade-off is modified when risk is evaluated more accurately by the probability of the gamble’s ruin.

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Optimal dormancy strategies in fluctuating environments given delays in phenotypic switching

Cited by 4 publications

References 24 publications

Phage infection fronts trigger early sporulation and collective defense in bacterial populations

Phage infection fronts trigger early sporulation and collective defense in bacterial populations

Onco-Breastomics: An Eco-Evo-Devo Holistic Approach

The trade-off between growth and risk in Kelly’s gambling and beyond

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