We study a model of contraction-based cell motility inside a microchannel to investigate the regulation of cell polarization and motion by the mechanical resistance of the environment. A positive feedback between the asymmetry of the acto-myosin cortex density and cell motion gives rise to a spontaneous symmetry breaking beyond a threshold contractility that depends on the resistance of extracellular medium. In highly viscous environments, we predict bistability under moderate contractility, so that symmetry breaking needs to be activated. In a viscoelastic environment, we find periodic oscillations in cortex density and velocity polarization. At the boundary between viscous and viscoelastic environments, the cell may either cross into the viscoelastic medium, bounce back into the viscous medium, or become trapped at the boundary. The different scenarios defined different phase diagram that are confirmed by numerical simulations.
{"title":"Contractility-driven cell motility against a viscoelastic resistance","authors":"Tapas Singha, Pierre Sens","doi":"arxiv-2402.17669","DOIUrl":"https://doi.org/arxiv-2402.17669","url":null,"abstract":"We study a model of contraction-based cell motility inside a microchannel to\u0000investigate the regulation of cell polarization and motion by the mechanical\u0000resistance of the environment. A positive feedback between the asymmetry of the\u0000acto-myosin cortex density and cell motion gives rise to a spontaneous symmetry\u0000breaking beyond a threshold contractility that depends on the resistance of\u0000extracellular medium. In highly viscous environments, we predict bistability\u0000under moderate contractility, so that symmetry breaking needs to be activated.\u0000In a viscoelastic environment, we find periodic oscillations in cortex density\u0000and velocity polarization. At the boundary between viscous and viscoelastic\u0000environments, the cell may either cross into the viscoelastic medium, bounce\u0000back into the viscous medium, or become trapped at the boundary. The different\u0000scenarios defined different phase diagram that are confirmed by numerical\u0000simulations.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140003500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The biochronometers used to keep time in eukaryotes include short-period biochronometer (SPB) and long-period biochronometer (LPB). Because the circadian clock reflects the biological time rhythm of a day, it is considered as SPB. Telomere shortening, which reflects the decreasing of telomere DNA length of chromosomes with the increase of cell division times, can be used to time the lifespan of organisms, so it is regarded as LPB. It is confirmed that SPB and LPB exist in most eukaryotes, and it is speculated that SPB and LPB are closely related. In this paper, based on existing studies, it is speculated that SPB and LPB of most eukaryotes can be co-attenuated with cell division in the process of aging. Due to the attenuated phenomenon of key components in the biochronometers during the growth and development of organisms, the biochronometers attenuate with the aging. Based on existing research results, it is preliminarily determined that the biochronometers can be rebuilt in the co-attenuated process. When the key components of biochronometers are reversed and increased in the organism, it can lead to the reversal of biochronometers, which further leads to the phenomenon of biological rejuvenation and makes the organism younger. In addition, the rebuilding of biochronometers can also lead to the acceleration of biochronometers and the shortening of the original timing time of biochronometers, thus shortening the life span of organisms. The rebuilding of biochronometers includes the reversal of biochronometers, the truncation of biochronometers timing and Uncoordinated co-attenuation of biochronometer and so on. The reversal of the biochronometers, which leads to rejuvenation, can give us a whole new understanding of life expectancy to be different from anti-aging.
真核生物用于计时的生物钟包括短周期生物钟（SPB）和长周期生物钟（LPB）。由于昼夜节律钟反映了一天的生物时间节律，因此被认为是 SPB。端粒缩短反映了染色体端粒 DNA 长度随着细胞分裂次数的增加而减少，可用于计算生物的寿命，因此被视为 LPB。研究证实，大多数真核生物都存在SPB和LPB，并推测SPB和LPB密切相关。本文在已有研究的基础上，推测大多数真核生物的 SPB 和 LPB 在衰老过程中会随着细胞分裂而共同衰减。由于在生物的生长发育过程中，生物同步器中的关键成分会出现衰减现象，因此生物同步器会随着衰老而衰减。根据已有的研究成果，初步判断生物钟可以在衰减过程中重建。当生物计时器的关键成分在机体内逆转和增加时，可导致生物计时器逆转，从而进一步导致生物年轻化现象，使机体更年轻。此外，生物钟的重建也会导致生物钟的加速，缩短生物钟的原始计时时间，从而缩短生物的寿命。生物同步器的构建包括生物同步器的逆转、生物同步器时间的截断和生物同步器的非协调共衰减等。生物时间计的逆转导致了生物的返老还童，可以让我们对预期寿命有一个全新的认识，从而有别于抗衰老。
{"title":"Rebuildable biochronometer: inferences and hypothesis on eukaryotic timing system","authors":"Ming-Jia Fu","doi":"arxiv-2402.16271","DOIUrl":"https://doi.org/arxiv-2402.16271","url":null,"abstract":"The biochronometers used to keep time in eukaryotes include short-period\u0000biochronometer (SPB) and long-period biochronometer (LPB). Because the\u0000circadian clock reflects the biological time rhythm of a day, it is considered\u0000as SPB. Telomere shortening, which reflects the decreasing of telomere DNA\u0000length of chromosomes with the increase of cell division times, can be used to\u0000time the lifespan of organisms, so it is regarded as LPB. It is confirmed that\u0000SPB and LPB exist in most eukaryotes, and it is speculated that SPB and LPB are\u0000closely related. In this paper, based on existing studies, it is speculated\u0000that SPB and LPB of most eukaryotes can be co-attenuated with cell division in\u0000the process of aging. Due to the attenuated phenomenon of key components in the\u0000biochronometers during the growth and development of organisms, the\u0000biochronometers attenuate with the aging. Based on existing research results,\u0000it is preliminarily determined that the biochronometers can be rebuilt in the\u0000co-attenuated process. When the key components of biochronometers are reversed\u0000and increased in the organism, it can lead to the reversal of biochronometers,\u0000which further leads to the phenomenon of biological rejuvenation and makes the\u0000organism younger. In addition, the rebuilding of biochronometers can also lead\u0000to the acceleration of biochronometers and the shortening of the original\u0000timing time of biochronometers, thus shortening the life span of organisms. The\u0000rebuilding of biochronometers includes the reversal of biochronometers, the\u0000truncation of biochronometers timing and Uncoordinated co-attenuation of\u0000biochronometer and so on. The reversal of the biochronometers, which leads to\u0000rejuvenation, can give us a whole new understanding of life expectancy to be\u0000different from anti-aging.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139977419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hyperbaric oxygen therapy (HBOT) proves vital in saving lives by elevating the partial pressure of oxygen (pO2). However, HBOT may also have toxic effects, including lung and retinal damage (peripheral HBOT toxicity), muscle spasms and violent myoclonic convulsions (CNS HBOT toxicity), which may even lead to death if left untreated. Despite the severity of the toxic effects of HBOT, their mechanism is only poorly understood to date. This lack of understanding the underlying mechanism hinders the development of new, effective therapies and preventive strategies to supress HBOT toxicity. Herein, we provide evidence that (1) increased pO2 increases the content of reactive oxygen species (ROS) in tissues, which causes peripheral HBOT toxicity and contributes to CNS toxicity by irreversibly altering cell receptors. Moreover, (2) increased ROS concentration in brain lowers activity of glutamic decarboxylase (GD), which lowers concentrations of inhibitory neurotransmitter gamma-aminobutyric acid (GABA), thereby contributing to the onset of HBOT-derived convulsions. At last, we provide long overlooked evidence that (3) elevated ambient pressure directly inhibits GABA(A) and glycine receptors, thereby leading to the rapid onset of HBOT-derived convulsions. We show that only a combination of these three mechanisms (1 + 2 + 3) are needed to explain most phenomena seen in HBOT toxicity (especially in CNS toxicity). Based on these proposed intertwined mechanisms, we propose administering antioxidants (lowering ROS concentrations), pyridoxine (restoring GD activity), and low doses of sedatives/ anaesthetics (reversing inhibitory effects of pressure on GABA(A) and glycine receptors) before routine hyperbaric oxygen therapies and deep-sea diving to prevent the HBOT toxicity.
{"title":"Mechanism and Prevention of Hyperbaric Oxygen Convulsions","authors":"Ondrej Groborz, Ludek Sefc, Petr Marsalek","doi":"arxiv-2402.14669","DOIUrl":"https://doi.org/arxiv-2402.14669","url":null,"abstract":"Hyperbaric oxygen therapy (HBOT) proves vital in saving lives by elevating\u0000the partial pressure of oxygen (pO2). However, HBOT may also have toxic\u0000effects, including lung and retinal damage (peripheral HBOT toxicity), muscle\u0000spasms and violent myoclonic convulsions (CNS HBOT toxicity), which may even\u0000lead to death if left untreated. Despite the severity of the toxic effects of\u0000HBOT, their mechanism is only poorly understood to date. This lack of\u0000understanding the underlying mechanism hinders the development of new,\u0000effective therapies and preventive strategies to supress HBOT toxicity. Herein,\u0000we provide evidence that (1) increased pO2 increases the content of reactive\u0000oxygen species (ROS) in tissues, which causes peripheral HBOT toxicity and\u0000contributes to CNS toxicity by irreversibly altering cell receptors. Moreover,\u0000(2) increased ROS concentration in brain lowers activity of glutamic\u0000decarboxylase (GD), which lowers concentrations of inhibitory neurotransmitter\u0000gamma-aminobutyric acid (GABA), thereby contributing to the onset of\u0000HBOT-derived convulsions. At last, we provide long overlooked evidence that (3)\u0000elevated ambient pressure directly inhibits GABA(A) and glycine receptors,\u0000thereby leading to the rapid onset of HBOT-derived convulsions. We show that\u0000only a combination of these three mechanisms (1 + 2 + 3) are needed to explain\u0000most phenomena seen in HBOT toxicity (especially in CNS toxicity). Based on\u0000these proposed intertwined mechanisms, we propose administering antioxidants\u0000(lowering ROS concentrations), pyridoxine (restoring GD activity), and low\u0000doses of sedatives/ anaesthetics (reversing inhibitory effects of pressure on\u0000GABA(A) and glycine receptors) before routine hyperbaric oxygen therapies and\u0000deep-sea diving to prevent the HBOT toxicity.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139946258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In this paper, we investigate the dynamics of hepatitis B virus infection taking into account the implementation of combination therapy through mathematical modeling. This model is established considering the interplay between uninfected cells, infected cells, capsids, and viruses. Three drugs are considered for specific roles (i) pegylated interferon (PEG IFN) for immune modulation, (ii) lamivudine (LMV) as a reverse-transcriptase inhibitor, and (iii) entecavir (ETV) to block capsid recycling. Using these drugs, three combination therapies are introduced, specifically CT PEG IFN plus LMV, CT PEG IFN plus ETV, and CT PEG IFN plus LMV plus ETV. As a result, when LMV is used in combination therapy with PEG IFN and ETV, the impacts of ETV become insignificant. In conclusion, if the appropriate drug effectively inhibits reverse transcription, there is no need for an additional inhibitor to block capsid recycling.
{"title":"Combination Therapy for Chronic Hepatitis B Using Capsid Recycling Inhibitor","authors":"Rupchand Sutradhar, D C Dalal","doi":"arxiv-2402.07701","DOIUrl":"https://doi.org/arxiv-2402.07701","url":null,"abstract":"In this paper, we investigate the dynamics of hepatitis B virus infection\u0000taking into account the implementation of combination therapy through\u0000mathematical modeling. This model is established considering the interplay\u0000between uninfected cells, infected cells, capsids, and viruses. Three drugs are\u0000considered for specific roles (i) pegylated interferon (PEG IFN) for immune\u0000modulation, (ii) lamivudine (LMV) as a reverse-transcriptase inhibitor, and\u0000(iii) entecavir (ETV) to block capsid recycling. Using these drugs, three\u0000combination therapies are introduced, specifically CT PEG IFN plus LMV, CT PEG\u0000IFN plus ETV, and CT PEG IFN plus LMV plus ETV. As a result, when LMV is used\u0000in combination therapy with PEG IFN and ETV, the impacts of ETV become\u0000insignificant. In conclusion, if the appropriate drug effectively inhibits\u0000reverse transcription, there is no need for an additional inhibitor to block\u0000capsid recycling.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139756887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Olfactory ensheathing glia (OEG) cells are known to foster axonal regeneration of central nervous system (CNS) neurons. Several lines of reversibly immortalized human OEG (ihOEG) have been previously established that enabled to develop models for their validation in vitro and in vivo. In this work, a constitutively GFP-expressing ihOEG cell line was obtained, and named Ts14-GFP. Ts14-GFP neuroregenerative ability was similar to that found for the parental line Ts14 and it can be assayed using in vivo transplantation experimental paradigms, after spinal cord or optic nerve damage. Additionally, we have engineered a low-regenerative ihOEG line, hTL2, using lentiviral transduction of the large T antigen from SV40 virus, denominated from now on Ts12. Ts12 can be used as a low regeneration control in these experiments.
{"title":"Transduction of an immortalized olfactory ensheathing glia cell line with the green fluorescent protein (GFP) gene: evaluation of its neuroregenerative capacity as a proof of concept","authors":"N Plaza, D Simón, J Sierra, MT Moreno-Flores","doi":"arxiv-2401.15133","DOIUrl":"https://doi.org/arxiv-2401.15133","url":null,"abstract":"Olfactory ensheathing glia (OEG) cells are known to foster axonal\u0000regeneration of central nervous system (CNS) neurons. Several lines of\u0000reversibly immortalized human OEG (ihOEG) have been previously established that\u0000enabled to develop models for their validation in vitro and in vivo. In this\u0000work, a constitutively GFP-expressing ihOEG cell line was obtained, and named\u0000Ts14-GFP. Ts14-GFP neuroregenerative ability was similar to that found for the\u0000parental line Ts14 and it can be assayed using in vivo transplantation\u0000experimental paradigms, after spinal cord or optic nerve damage. Additionally,\u0000we have engineered a low-regenerative ihOEG line, hTL2, using lentiviral\u0000transduction of the large T antigen from SV40 virus, denominated from now on\u0000Ts12. Ts12 can be used as a low regeneration control in these experiments.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139585976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sensory adaptation enables organisms to adjust their perception in a changing environment. A paradigm is bacterial chemotaxis, where the output activity of chemoreceptors is adapted to different baseline concentrations via receptor methylation. The range of internal receptor states limits the stimulus magnitude to which these systems can adapt. Here, we employ a highly idealized, Langevin-equation based model to study how the finite range of state variables affects the adaptation accuracy and the energy dissipation in individual and coupled systems. Maintaining an adaptive state requires constant energy dissipation. We show that the steady-state dissipation rate increases approximately linearly with the adaptation accuracy for varying stimulus magnitudes in the so-called perfect adaptation limit. This result complements the well-known logarithmic cost-accuracy relationship for varying chemical driving. Next, we study linearly coupled pairs of sensory units. We find that the interaction reduces the dissipation rate per unit and affects the overall cost-accuracy relationship. A coupling of the slow methylation variables results in a better accuracy than a coupling of activities. Overall, the findings highlight the significance of both the working range and collective operation mode as crucial design factors that impact the accuracy and energy expenditure of molecular adaptation networks.
{"title":"Sensory adaptation in a continuum model of bacterial chemotaxis -- working range, cost-accuracy relation, and coupled systems","authors":"Vansh Kharbanda, Benedikt Sabass","doi":"arxiv-2401.11341","DOIUrl":"https://doi.org/arxiv-2401.11341","url":null,"abstract":"Sensory adaptation enables organisms to adjust their perception in a changing\u0000environment. A paradigm is bacterial chemotaxis, where the output activity of\u0000chemoreceptors is adapted to different baseline concentrations via receptor\u0000methylation. The range of internal receptor states limits the stimulus\u0000magnitude to which these systems can adapt. Here, we employ a highly idealized,\u0000Langevin-equation based model to study how the finite range of state variables\u0000affects the adaptation accuracy and the energy dissipation in individual and\u0000coupled systems. Maintaining an adaptive state requires constant energy\u0000dissipation. We show that the steady-state dissipation rate increases\u0000approximately linearly with the adaptation accuracy for varying stimulus\u0000magnitudes in the so-called perfect adaptation limit. This result complements\u0000the well-known logarithmic cost-accuracy relationship for varying chemical\u0000driving. Next, we study linearly coupled pairs of sensory units. We find that\u0000the interaction reduces the dissipation rate per unit and affects the overall\u0000cost-accuracy relationship. A coupling of the slow methylation variables\u0000results in a better accuracy than a coupling of activities. Overall, the\u0000findings highlight the significance of both the working range and collective\u0000operation mode as crucial design factors that impact the accuracy and energy\u0000expenditure of molecular adaptation networks.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139557105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
James P. Conboy, Irene Istúriz Petitjean, Anouk van der Net, Gijsje H. Koenderink
Cell migration is a fundamental process for life and is highly dependent on the dynamical and mechanical properties of the cytoskeleton. Intensive physical and biochemical crosstalk between actin, microtubules, and intermediate filaments ensures their coordination to facilitate and enable migration. In this review we discuss the different mechanical aspects that govern cell migration and provide, for each mechanical aspect, a novel perspective by juxtaposing two complementary approaches to the biophysical study of cytoskeletal crosstalk: live-cell studies (often referred to as top-down studies) and cell-free studies (often referred to as bottom-up studies). We summarize the main findings from both experimental approaches, and we provide our perspective on bridging the two perspectives to address the open questions of how cytoskeletal crosstalk governs cell migration and makes cells move.
{"title":"How cytoskeletal crosstalk makes cells move: bridging cell-free and cell studies","authors":"James P. Conboy, Irene Istúriz Petitjean, Anouk van der Net, Gijsje H. Koenderink","doi":"arxiv-2401.08368","DOIUrl":"https://doi.org/arxiv-2401.08368","url":null,"abstract":"Cell migration is a fundamental process for life and is highly dependent on\u0000the dynamical and mechanical properties of the cytoskeleton. Intensive physical\u0000and biochemical crosstalk between actin, microtubules, and intermediate\u0000filaments ensures their coordination to facilitate and enable migration. In\u0000this review we discuss the different mechanical aspects that govern cell\u0000migration and provide, for each mechanical aspect, a novel perspective by\u0000juxtaposing two complementary approaches to the biophysical study of\u0000cytoskeletal crosstalk: live-cell studies (often referred to as top-down\u0000studies) and cell-free studies (often referred to as bottom-up studies). We\u0000summarize the main findings from both experimental approaches, and we provide\u0000our perspective on bridging the two perspectives to address the open questions\u0000of how cytoskeletal crosstalk governs cell migration and makes cells move.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139481376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rebecca M. Crossley, Kevin J. Painter, Tommaso Lorenzi, Philip K. Maini, Ruth E. Baker
A fundamental feature of collective cell migration is phenotypic heterogeneity which, for example, influences tumour progression and relapse. While current mathematical models often consider discrete phenotypic structuring of the cell population, in-line with the `go-or-grow' hypothesis cite{hatzikirou2012go, stepien2018traveling}, they regularly overlook the role that the environment may play in determining the cells' phenotype during migration. Comparing a previously studied volume-filling model for a homogeneous population of generalist cells that can proliferate, move and degrade extracellular matrix (ECM) cite{crossley2023travelling} to a novel model for a heterogeneous population comprising two distinct sub-populations of specialist cells that can either move and degrade ECM or proliferate, this study explores how different hypothetical phenotypic switching mechanisms affect the speed and structure of the invading cell populations. Through a continuum model derived from its individual-based counterpart, insights into the influence of the ECM and the impact of phenotypic switching on migrating cell populations emerge. Notably, specialist cell populations that cannot switch phenotype show reduced invasiveness compared to generalist cell populations, while implementing different forms of switching significantly alters the structure of migrating cell fronts. This key result suggests that the structure of an invading cell population could be used to infer the underlying mechanisms governing phenotypic switching.
{"title":"Phenotypic switching mechanisms determine the structure of cell migration into extracellular matrix under the `go-or-grow' hypothesis","authors":"Rebecca M. Crossley, Kevin J. Painter, Tommaso Lorenzi, Philip K. Maini, Ruth E. Baker","doi":"arxiv-2401.07279","DOIUrl":"https://doi.org/arxiv-2401.07279","url":null,"abstract":"A fundamental feature of collective cell migration is phenotypic\u0000heterogeneity which, for example, influences tumour progression and relapse.\u0000While current mathematical models often consider discrete phenotypic\u0000structuring of the cell population, in-line with the `go-or-grow' hypothesis\u0000cite{hatzikirou2012go, stepien2018traveling}, they regularly overlook the role\u0000that the environment may play in determining the cells' phenotype during\u0000migration. Comparing a previously studied volume-filling model for a\u0000homogeneous population of generalist cells that can proliferate, move and\u0000degrade extracellular matrix (ECM) cite{crossley2023travelling} to a novel\u0000model for a heterogeneous population comprising two distinct sub-populations of\u0000specialist cells that can either move and degrade ECM or proliferate, this\u0000study explores how different hypothetical phenotypic switching mechanisms\u0000affect the speed and structure of the invading cell populations. Through a\u0000continuum model derived from its individual-based counterpart, insights into\u0000the influence of the ECM and the impact of phenotypic switching on migrating\u0000cell populations emerge. Notably, specialist cell populations that cannot\u0000switch phenotype show reduced invasiveness compared to generalist cell\u0000populations, while implementing different forms of switching significantly\u0000alters the structure of migrating cell fronts. This key result suggests that\u0000the structure of an invading cell population could be used to infer the\u0000underlying mechanisms governing phenotypic switching.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139481323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A stochastic model is used to assess the effect of external parameters on the development of submerged biofilms on smooth and rough surfaces. The model includes basic cellular mechanisms, such as division and spreading, together with an elementary description of the interaction with the surrounding flow and probabilistic rules for EPS matrix generation, cell decay and adhesion. Insight on the interplay of competing mechanisms as the flow or the nutrient concentration change is gained. Erosion and growth processes combined produce biofilm structures moving downstream. A rich variety of patterns are generated: shrinking biofilms, patches, ripple-like structures traveling downstream, fingers, mounds, streamer-like patterns, flat layers, porous and dendritic structures. The observed regimes depend on the carbon source and the type of bacteria.
{"title":"Biofilm growth on rugose surfaces","authors":"David Rodriguez, Baldvin Einarsson, Ana Carpio","doi":"arxiv-2401.07135","DOIUrl":"https://doi.org/arxiv-2401.07135","url":null,"abstract":"A stochastic model is used to assess the effect of external parameters on the\u0000development of submerged biofilms on smooth and rough surfaces. The model\u0000includes basic cellular mechanisms, such as division and spreading, together\u0000with an elementary description of the interaction with the surrounding flow and\u0000probabilistic rules for EPS matrix generation, cell decay and adhesion. Insight\u0000on the interplay of competing mechanisms as the flow or the nutrient\u0000concentration change is gained. Erosion and growth processes combined produce\u0000biofilm structures moving downstream. A rich variety of patterns are generated:\u0000shrinking biofilms, patches, ripple-like structures traveling downstream,\u0000fingers, mounds, streamer-like patterns, flat layers, porous and dendritic\u0000structures. The observed regimes depend on the carbon source and the type of\u0000bacteria.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139480990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The dynamics of cellular aggregates is driven by the interplay of mechanochemical processes and cellular activity. Although deterministic models may capture mechanical features, local chemical fluctuations trigger random cell responses, which determine the overall evolution. Incorporating stochastic cellular behavior in macroscopic models of biological media is a challenging task. Herein, we propose hybrid models for bacterial biofilm growth, which couple a two phase solid/fluid mixture description of mechanical and chemical fields with a dynamic energy budget-based cellular automata treatment of bacterial activity. Thin film and plate approximations for the relevant interfaces allow us to obtain numerical solutions exhibiting behaviors observed in experiments, such as accelerated spread due to water intake from the environment, wrinkle formation, undulated contour development, and the appearance of inhomogeneous distributions of differentiated bacteria performing varied tasks.
{"title":"Incorporating Cellular Stochasticity in Solid--Fluid Mixture Biofilm Models","authors":"Ana Carpio, Elena Cebrian","doi":"arxiv-2401.07088","DOIUrl":"https://doi.org/arxiv-2401.07088","url":null,"abstract":"The dynamics of cellular aggregates is driven by the interplay of\u0000mechanochemical processes and cellular activity. Although deterministic models\u0000may capture mechanical features, local chemical fluctuations trigger random\u0000cell responses, which determine the overall evolution. Incorporating stochastic\u0000cellular behavior in macroscopic models of biological media is a challenging\u0000task. Herein, we propose hybrid models for bacterial biofilm growth, which\u0000couple a two phase solid/fluid mixture description of mechanical and chemical\u0000fields with a dynamic energy budget-based cellular automata treatment of\u0000bacterial activity. Thin film and plate approximations for the relevant\u0000interfaces allow us to obtain numerical solutions exhibiting behaviors observed\u0000in experiments, such as accelerated spread due to water intake from the\u0000environment, wrinkle formation, undulated contour development, and the\u0000appearance of inhomogeneous distributions of differentiated bacteria performing\u0000varied tasks.","PeriodicalId":501321,"journal":{"name":"arXiv - QuanBio - Cell Behavior","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139480988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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