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Regulatory mechanisms link phenotypic plasticity to evolvability.

van Gestel J, Weissing FJ - Sci Rep (2016)

Bottom Line: Using individual-based simulations, we compare the RN and GRN approach and find a number of striking differences.Most importantly, the GRN model results in a much higher diversity of responsive strategies than the RN model.The regulatory mechanisms that control plasticity therefore critically link phenotypic plasticity to the adaptive potential of biological populations.

View Article: PubMed Central - PubMed

Affiliation: Groningen Institute for Evolutionary Life Sciences, University of Groningen, P.O. Box 11103, Groningen 9700 CC, The Netherlands.

ABSTRACT
Organisms have a remarkable capacity to respond to environmental change. They can either respond directly, by means of phenotypic plasticity, or they can slowly adapt through evolution. Yet, how phenotypic plasticity links to evolutionary adaptability is largely unknown. Current studies of plasticity tend to adopt a phenomenological reaction norm (RN) approach, which neglects the mechanisms underlying plasticity. Focusing on a concrete question - the optimal timing of bacterial sporulation - we here also consider a mechanistic approach, the evolution of a gene regulatory network (GRN) underlying plasticity. Using individual-based simulations, we compare the RN and GRN approach and find a number of striking differences. Most importantly, the GRN model results in a much higher diversity of responsive strategies than the RN model. We show that each of the evolved strategies is pre-adapted to a unique set of unseen environmental conditions. The regulatory mechanisms that control plasticity therefore critically link phenotypic plasticity to the adaptive potential of biological populations.

No MeSH data available.


Related in: MedlinePlus

Evolution of sporulation in the RN model.(Left) Number of cells (blue) and spores (red) in 500 replicate simulations over the course of 400 generations. At each generation, cell and spore counts are collected at the end of colony growth. The black lines show the average number of cells and spores. (middle) Distributions of the number of cells and spores over the 500 replicate simulations at the end of evolution. (right) Colonies of the most productive genotype at generation 1, 200 and 400.
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f3: Evolution of sporulation in the RN model.(Left) Number of cells (blue) and spores (red) in 500 replicate simulations over the course of 400 generations. At each generation, cell and spore counts are collected at the end of colony growth. The black lines show the average number of cells and spores. (middle) Distributions of the number of cells and spores over the 500 replicate simulations at the end of evolution. (right) Colonies of the most productive genotype at generation 1, 200 and 400.

Mentions: We first examine the evolution of plasticity in the RN model. Figure 3 shows the number of cells and spores in the 500 replicate simulations over the course of 400 generations. Since at the onset of evolution cells are unable to sporulate, the colonies in the first generation do not produce spores, with the exception of some mutants. Over evolutionary time, sporulation evolves and the number of spores that are present at the end of colony growth increases (Fig. 3). At the same time the colony size decreases, because energy that is allocated to sporulation cannot be used for cell division. Despite the smaller colonies, the evolved genotypes have a higher fitness than their non-sporulating ancestors, because spores are more likely to survive dispersal than cells. The colony at generation 200 is characterized by two radial zones: the center and the edge. Spores mostly occur in the colony center, where nutrients are depleted first, while dividing cells occur at the colony edge. From generation 200 onwards, the colonies of most replicate simulations produce a constant number of spores until the end of evolution. Interestingly, when examining the distribution of spore production among the 500 replicate simulations, one can discriminate three phenotypic groups: colonies that produce a low (~600 spores), intermediate (~800) and high (~1,200) number of spores. Since the colonies belong to separate replicate simulations, we hypothesized that three phenotypic groups belong to separate evolutionary trajectories, each trajectory leading to another level of spore production.


Regulatory mechanisms link phenotypic plasticity to evolvability.

van Gestel J, Weissing FJ - Sci Rep (2016)

Evolution of sporulation in the RN model.(Left) Number of cells (blue) and spores (red) in 500 replicate simulations over the course of 400 generations. At each generation, cell and spore counts are collected at the end of colony growth. The black lines show the average number of cells and spores. (middle) Distributions of the number of cells and spores over the 500 replicate simulations at the end of evolution. (right) Colonies of the most productive genotype at generation 1, 200 and 400.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4834480&req=5

f3: Evolution of sporulation in the RN model.(Left) Number of cells (blue) and spores (red) in 500 replicate simulations over the course of 400 generations. At each generation, cell and spore counts are collected at the end of colony growth. The black lines show the average number of cells and spores. (middle) Distributions of the number of cells and spores over the 500 replicate simulations at the end of evolution. (right) Colonies of the most productive genotype at generation 1, 200 and 400.
Mentions: We first examine the evolution of plasticity in the RN model. Figure 3 shows the number of cells and spores in the 500 replicate simulations over the course of 400 generations. Since at the onset of evolution cells are unable to sporulate, the colonies in the first generation do not produce spores, with the exception of some mutants. Over evolutionary time, sporulation evolves and the number of spores that are present at the end of colony growth increases (Fig. 3). At the same time the colony size decreases, because energy that is allocated to sporulation cannot be used for cell division. Despite the smaller colonies, the evolved genotypes have a higher fitness than their non-sporulating ancestors, because spores are more likely to survive dispersal than cells. The colony at generation 200 is characterized by two radial zones: the center and the edge. Spores mostly occur in the colony center, where nutrients are depleted first, while dividing cells occur at the colony edge. From generation 200 onwards, the colonies of most replicate simulations produce a constant number of spores until the end of evolution. Interestingly, when examining the distribution of spore production among the 500 replicate simulations, one can discriminate three phenotypic groups: colonies that produce a low (~600 spores), intermediate (~800) and high (~1,200) number of spores. Since the colonies belong to separate replicate simulations, we hypothesized that three phenotypic groups belong to separate evolutionary trajectories, each trajectory leading to another level of spore production.

Bottom Line: Using individual-based simulations, we compare the RN and GRN approach and find a number of striking differences.Most importantly, the GRN model results in a much higher diversity of responsive strategies than the RN model.The regulatory mechanisms that control plasticity therefore critically link phenotypic plasticity to the adaptive potential of biological populations.

View Article: PubMed Central - PubMed

Affiliation: Groningen Institute for Evolutionary Life Sciences, University of Groningen, P.O. Box 11103, Groningen 9700 CC, The Netherlands.

ABSTRACT
Organisms have a remarkable capacity to respond to environmental change. They can either respond directly, by means of phenotypic plasticity, or they can slowly adapt through evolution. Yet, how phenotypic plasticity links to evolutionary adaptability is largely unknown. Current studies of plasticity tend to adopt a phenomenological reaction norm (RN) approach, which neglects the mechanisms underlying plasticity. Focusing on a concrete question - the optimal timing of bacterial sporulation - we here also consider a mechanistic approach, the evolution of a gene regulatory network (GRN) underlying plasticity. Using individual-based simulations, we compare the RN and GRN approach and find a number of striking differences. Most importantly, the GRN model results in a much higher diversity of responsive strategies than the RN model. We show that each of the evolved strategies is pre-adapted to a unique set of unseen environmental conditions. The regulatory mechanisms that control plasticity therefore critically link phenotypic plasticity to the adaptive potential of biological populations.

No MeSH data available.


Related in: MedlinePlus