ABSTRACT
[This corrects the article DOI: 10.1371/journal.pbio.1002540.].
ABSTRACT
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.
Subject(s)
Leucine/metabolism , Saccharomyces cerevisiae/metabolism , Symbiosis , Tryptophan/metabolism , Algorithms , Cell Division/drug effects , Cell Division/genetics , Culture Media/metabolism , Culture Media/pharmacology , Ecosystem , Flow Cytometry , Leucine/genetics , Metabolic Engineering/methods , Models, Biological , Saccharomyces cerevisiae/classification , Saccharomyces cerevisiae/genetics , Species Specificity , Spectrophotometry , Time Factors , Tryptophan/geneticsABSTRACT
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.
Subject(s)
Escherichia coli/drug effects , Gene Transfer, Horizontal/drug effects , Plasmids/metabolism , Quorum Sensing/genetics , beta-Lactam Resistance/drug effects , Ampicillin/pharmacology , Anti-Bacterial Agents/pharmacology , Bacterial Load/drug effects , Escherichia coli/enzymology , Escherichia coli/genetics , Models, Genetic , Plasmids/agonists , beta-Lactam Resistance/genetics , beta-Lactamase Inhibitors , beta-Lactamases/genetics , beta-Lactamases/metabolismABSTRACT
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.
