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Modeling Invasion Dynamics with Spatial Random-Fitness Due to Micro-Environment

Numerous experimental studies have demonstrated that the microenvironment is a key regulator influencing the proliferative and migrative potentials of species. Spatial and temporal disturbances lead to adverse and hazardous microenvironments for cellular systems that is reflected in the phenotypic h...

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Autores principales: Manem, V. S. K., Kaveh, K., Kohandel, M., Sivaloganathan, S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4624969/
https://www.ncbi.nlm.nih.gov/pubmed/26509572
http://dx.doi.org/10.1371/journal.pone.0140234
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author Manem, V. S. K.
Kaveh, K.
Kohandel, M.
Sivaloganathan, S.
author_facet Manem, V. S. K.
Kaveh, K.
Kohandel, M.
Sivaloganathan, S.
author_sort Manem, V. S. K.
collection PubMed
description Numerous experimental studies have demonstrated that the microenvironment is a key regulator influencing the proliferative and migrative potentials of species. Spatial and temporal disturbances lead to adverse and hazardous microenvironments for cellular systems that is reflected in the phenotypic heterogeneity within the system. In this paper, we study the effect of microenvironment on the invasive capability of species, or mutants, on structured grids (in particular, square lattices) under the influence of site-dependent random proliferation in addition to a migration potential. We discuss both continuous and discrete fitness distributions. Our results suggest that the invasion probability is negatively correlated with the variance of fitness distribution of mutants (for both advantageous and neutral mutants) in the absence of migration of both types of cells. A similar behaviour is observed even in the presence of a random fitness distribution of host cells in the system with neutral fitness rate. In the case of a bimodal distribution, we observe zero invasion probability until the system reaches a (specific) proportion of advantageous phenotypes. Also, we find that the migrative potential amplifies the invasion probability as the variance of fitness of mutants increases in the system, which is the exact opposite in the absence of migration. Our computational framework captures the harsh microenvironmental conditions through quenched random fitness distributions and migration of cells, and our analysis shows that they play an important role in the invasion dynamics of several biological systems such as bacterial micro-habitats, epithelial dysplasia, and metastasis. We believe that our results may lead to more experimental studies, which can in turn provide further insights into the role and impact of heterogeneous environments on invasion dynamics.
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spelling pubmed-46249692015-11-06 Modeling Invasion Dynamics with Spatial Random-Fitness Due to Micro-Environment Manem, V. S. K. Kaveh, K. Kohandel, M. Sivaloganathan, S. PLoS One Research Article Numerous experimental studies have demonstrated that the microenvironment is a key regulator influencing the proliferative and migrative potentials of species. Spatial and temporal disturbances lead to adverse and hazardous microenvironments for cellular systems that is reflected in the phenotypic heterogeneity within the system. In this paper, we study the effect of microenvironment on the invasive capability of species, or mutants, on structured grids (in particular, square lattices) under the influence of site-dependent random proliferation in addition to a migration potential. We discuss both continuous and discrete fitness distributions. Our results suggest that the invasion probability is negatively correlated with the variance of fitness distribution of mutants (for both advantageous and neutral mutants) in the absence of migration of both types of cells. A similar behaviour is observed even in the presence of a random fitness distribution of host cells in the system with neutral fitness rate. In the case of a bimodal distribution, we observe zero invasion probability until the system reaches a (specific) proportion of advantageous phenotypes. Also, we find that the migrative potential amplifies the invasion probability as the variance of fitness of mutants increases in the system, which is the exact opposite in the absence of migration. Our computational framework captures the harsh microenvironmental conditions through quenched random fitness distributions and migration of cells, and our analysis shows that they play an important role in the invasion dynamics of several biological systems such as bacterial micro-habitats, epithelial dysplasia, and metastasis. We believe that our results may lead to more experimental studies, which can in turn provide further insights into the role and impact of heterogeneous environments on invasion dynamics. Public Library of Science 2015-10-28 /pmc/articles/PMC4624969/ /pubmed/26509572 http://dx.doi.org/10.1371/journal.pone.0140234 Text en © 2015 Manem et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Manem, V. S. K.
Kaveh, K.
Kohandel, M.
Sivaloganathan, S.
Modeling Invasion Dynamics with Spatial Random-Fitness Due to Micro-Environment
title Modeling Invasion Dynamics with Spatial Random-Fitness Due to Micro-Environment
title_full Modeling Invasion Dynamics with Spatial Random-Fitness Due to Micro-Environment
title_fullStr Modeling Invasion Dynamics with Spatial Random-Fitness Due to Micro-Environment
title_full_unstemmed Modeling Invasion Dynamics with Spatial Random-Fitness Due to Micro-Environment
title_short Modeling Invasion Dynamics with Spatial Random-Fitness Due to Micro-Environment
title_sort modeling invasion dynamics with spatial random-fitness due to micro-environment
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4624969/
https://www.ncbi.nlm.nih.gov/pubmed/26509572
http://dx.doi.org/10.1371/journal.pone.0140234
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