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1.
PLoS Biol ; 15(6): e1002606, 2017 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-28591227

RESUMEN

[This corrects the article DOI: 10.1371/journal.pbio.1002540.].

2.
PLoS Biol ; 14(8): e1002540, 2016 08.
Artículo en Inglés | MEDLINE | ID: mdl-27557335

RESUMEN

Mutualisms between species play an important role in ecosystem function and stability. However, in some environments, the competitive aspects of an interaction may dominate the mutualistic aspects. Although these transitions could have far-reaching implications, it has been difficult to study the causes and consequences of this mutualistic-competitive transition in experimentally tractable systems. Here, we study a microbial cross-feeding mutualism in which each yeast strain supplies an essential amino acid for its partner strain. We find that, depending upon the amount of freely available amino acid in the environment, this pair of strains can exhibit an obligatory mutualism, facultative mutualism, competition, parasitism, competitive exclusion, or failed mutualism leading to extinction of the population. A simple model capturing the essential features of this interaction explains how resource availability modulates the interaction and predicts that changes in the dynamics of the mutualism in deteriorating environments can provide advance warning that collapse of the mutualism is imminent. We confirm this prediction experimentally by showing that, in the high nutrient competitive regime, the strains rapidly reach a common carrying capacity before slowly reaching the equilibrium ratio between the strains. However, in the low nutrient regime, before collapse of the obligate mutualism, we find that the ratio rapidly reaches its equilibrium and it is the total abundance that is slow to reach equilibrium. Our results provide a general framework for how mutualisms may transition between qualitatively different regimes of interaction in response to changes in nutrient availability in the environment.


Asunto(s)
Leucina/metabolismo , Saccharomyces cerevisiae/metabolismo , Simbiosis , Triptófano/metabolismo , Algoritmos , División Celular/efectos de los fármacos , División Celular/genética , Medios de Cultivo/metabolismo , Medios de Cultivo/farmacología , Ecosistema , Citometría de Flujo , Leucina/genética , Ingeniería Metabólica/métodos , Modelos Biológicos , Saccharomyces cerevisiae/clasificación , Saccharomyces cerevisiae/genética , Especificidad de la Especie , Espectrofotometría , Factores de Tiempo , Triptófano/genética
3.
Mol Syst Biol ; 9: 683, 2013 Aug 06.
Artículo en Inglés | MEDLINE | ID: mdl-23917989

RESUMEN

Inactivation of ß-lactam antibiotics by resistant bacteria is a 'cooperative' behavior that may allow sensitive bacteria to survive antibiotic treatment. However, the factors that determine the fraction of resistant cells in the bacterial population remain unclear, indicating a fundamental gap in our understanding of how antibiotic resistance evolves. Here, we experimentally track the spread of a plasmid that encodes a ß-lactamase enzyme through the bacterial population. We find that independent of the initial fraction of resistant cells, the population settles to an equilibrium fraction proportional to the antibiotic concentration divided by the cell density. A simple model explains this behavior, successfully predicting a data collapse over two orders of magnitude in antibiotic concentration. This model also successfully predicts that adding a commonly used ß-lactamase inhibitor will lead to the spread of resistance, highlighting the need to incorporate social dynamics into the study of antibiotic resistance.


Asunto(s)
Escherichia coli/efectos de los fármacos , Transferencia de Gen Horizontal/efectos de los fármacos , Plásmidos/metabolismo , Percepción de Quorum/genética , Resistencia betalactámica/efectos de los fármacos , Ampicilina/farmacología , Antibacterianos/farmacología , Carga Bacteriana/efectos de los fármacos , Escherichia coli/enzimología , Escherichia coli/genética , Modelos Genéticos , Plásmidos/agonistas , Resistencia betalactámica/genética , Inhibidores de beta-Lactamasas , beta-Lactamasas/genética , beta-Lactamasas/metabolismo
4.
Rev Sci Instrum ; 80(5): 054303, 2009 May.
Artículo en Inglés | MEDLINE | ID: mdl-19485522

RESUMEN

Tissue mechanical properties reflect extracellular matrix composition and organization, and as such, their changes can be a signature of disease. Examples of such diseases include intervertebral disk degeneration, cancer, atherosclerosis, osteoarthritis, osteoporosis, and tooth decay. Here we introduce the tissue diagnostic instrument (TDI), a device designed to probe the mechanical properties of normal and diseased soft and hard tissues not only in the laboratory but also in patients. The TDI can distinguish between the nucleus and the annulus of spinal disks, between young and degenerated cartilage, and between normal and cancerous mammary glands. It can quantify the elastic modulus and hardness of the wet dentin left in a cavity after excavation. It can perform an indentation test of bone tissue, quantifying the indentation depth increase and other mechanical parameters. With local anesthesia and disposable, sterile, probe assemblies, there has been neither pain nor complications in tests on patients. We anticipate that this unique device will facilitate research on many tissue systems in living organisms, including plants, leading to new insights into disease mechanisms and methods for their early detection.


Asunto(s)
Equipo para Diagnóstico , Animales , Fenómenos Biomecánicos , Cartílago/citología , Cartílago/patología , Dentina/citología , Dentina/patología , Humanos , Procesamiento de Imagen Asistido por Computador , Disco Intervertebral/citología , Disco Intervertebral/patología , Glándulas Mamarias Humanas/citología , Glándulas Mamarias Humanas/patología , Ratones
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