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Phenotype/genotype sequence complementarity and prebiotic replicator coexistence in the metabolically coupled replicator system.

Könnyű B, Czárán T - BMC Evol. Biol. (2014)

Bottom Line: The fact that RNA templates and their copies are of complementary base sequences has an obvious dynamical relevance: complementary strains may have very different structures and, consequently, functions - one may specialize for increasing enzymatic activity while the other takes the role of the gene of the enzyme.This asymmetry is expected to reverse due to the evolved trade-off of high "gene" replicability and high catalytic activity of the corresponding "enzyme" in expense of its replicability.This trade-off is the first evolutionary step towards the "division of labour" among enzymes and genes, which has concluded in the extreme form of phenotype amplification characteristic of our recent DNA-RNA-protein World.

View Article: PubMed Central - PubMed

ABSTRACT

Background: RNA or RNA-like polymers are the most likely candidates for having played the lead roles on the stage of the origin of life. RNA is known to feature two of the three essential functions of living entities (metabolism, heredity and membrane): it is capable of unlimited heredity and it has a proven capacity for catalysing very different chemical reactions which may form simple metabolic networks. The Metabolically Coupled Replicator System is a class of simulation models built on these two functions to show that an RNA World scenario for the origin of life is ecologically feasible, provided that it is played on mineral surfaces. The fact that RNA templates and their copies are of complementary base sequences has an obvious dynamical relevance: complementary strains may have very different structures and, consequently, functions - one may specialize for increasing enzymatic activity while the other takes the role of the gene of the enzyme.

Results: Incorporating the functional divergence of template and copy into the Metabolically Coupled Replicator System model framework we show that sequence complementarity 1) does not ruin the coexistence of a set of metabolically cooperating replicators; 2) the replicator system remains resistant to, but also tolerant with its parasites; 3) opens the way to the evolutionary differentiation of phenotype and genotype through a primitive version of phenotype amplification.

Conclusions: The functional asymmetry of complementary RNA strains results in a shift of phenotype/genotype (enzyme/gene) proportions in MCRS, favouring a slight genotype dominance. This asymmetry is expected to reverse due to the evolved trade-off of high "gene" replicability and high catalytic activity of the corresponding "enzyme" in expense of its replicability. This trade-off is the first evolutionary step towards the "division of labour" among enzymes and genes, which has concluded in the extreme form of phenotype amplification characteristic of our recent DNA-RNA-protein World.

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Coexistence of metabolic replicators in Model II. The rows of the figure differ in the number of diffusion steps per update: first row: D = 0, second row: D = 4; third row: D = 100. x- and y-axes are the sizes of metabolic (h) and replication (r) neighbourhood, respectively (N: von Neumann neighbourhood; 3: 3×3, 5: 5×5, 7: 7×7, 25: 25×25 and 37: 37×37 Moore neighbourhoods). The gray-scale shades of the boxes correspond to average replicator densities (%, see scale bar) on the whole grid at the end of the simulations (at t = 1.000). The numbers within the boxes of the panels indicate the average ratio (%) of the numbers of phenotype- and genotype forms at the end of the simulations (100 × Phenx/Genx, x = 1, .., 4) in five replicate runs of the simulation in each parameter set. Zero means the collapse of the system (no replicator survives to t = 1.000). Replication constants: k1p = 3.0, k1g = 4.0, k2p = 5.0, k2g = 6.0 , k3p = 7.0, k3g = 8.0, k4p = 9.0 and k4g = 10.0; subscripts p and g denote phenotype-forms and genotype-forms of replicator types, respectively.
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Fig4: Coexistence of metabolic replicators in Model II. The rows of the figure differ in the number of diffusion steps per update: first row: D = 0, second row: D = 4; third row: D = 100. x- and y-axes are the sizes of metabolic (h) and replication (r) neighbourhood, respectively (N: von Neumann neighbourhood; 3: 3×3, 5: 5×5, 7: 7×7, 25: 25×25 and 37: 37×37 Moore neighbourhoods). The gray-scale shades of the boxes correspond to average replicator densities (%, see scale bar) on the whole grid at the end of the simulations (at t = 1.000). The numbers within the boxes of the panels indicate the average ratio (%) of the numbers of phenotype- and genotype forms at the end of the simulations (100 × Phenx/Genx, x = 1, .., 4) in five replicate runs of the simulation in each parameter set. Zero means the collapse of the system (no replicator survives to t = 1.000). Replication constants: k1p = 3.0, k1g = 4.0, k2p = 5.0, k2g = 6.0 , k3p = 7.0, k3g = 8.0, k4p = 9.0 and k4g = 10.0; subscripts p and g denote phenotype-forms and genotype-forms of replicator types, respectively.

Mentions: Wherever the system is persistent, its equilibrium state can be fully specified by the stationary densities of the replicator species, and the phenotype to genotype density ratio within each species. Figures 2 and 3 summarize these output data obtained with Model I to demonstrate the effect of gene/enzyme functional complementarity devoid of the replicability difference between the “enzyme” and the “gene” form of the same replicator type, without and with a parasite, respectively; Figures 4 and 5 show the same simulation outcomes for Model II. The data shown on the figures are the averages of five replicate simulations for each parameter setting.Figure 2


Phenotype/genotype sequence complementarity and prebiotic replicator coexistence in the metabolically coupled replicator system.

Könnyű B, Czárán T - BMC Evol. Biol. (2014)

Coexistence of metabolic replicators in Model II. The rows of the figure differ in the number of diffusion steps per update: first row: D = 0, second row: D = 4; third row: D = 100. x- and y-axes are the sizes of metabolic (h) and replication (r) neighbourhood, respectively (N: von Neumann neighbourhood; 3: 3×3, 5: 5×5, 7: 7×7, 25: 25×25 and 37: 37×37 Moore neighbourhoods). The gray-scale shades of the boxes correspond to average replicator densities (%, see scale bar) on the whole grid at the end of the simulations (at t = 1.000). The numbers within the boxes of the panels indicate the average ratio (%) of the numbers of phenotype- and genotype forms at the end of the simulations (100 × Phenx/Genx, x = 1, .., 4) in five replicate runs of the simulation in each parameter set. Zero means the collapse of the system (no replicator survives to t = 1.000). Replication constants: k1p = 3.0, k1g = 4.0, k2p = 5.0, k2g = 6.0 , k3p = 7.0, k3g = 8.0, k4p = 9.0 and k4g = 10.0; subscripts p and g denote phenotype-forms and genotype-forms of replicator types, respectively.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
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Fig4: Coexistence of metabolic replicators in Model II. The rows of the figure differ in the number of diffusion steps per update: first row: D = 0, second row: D = 4; third row: D = 100. x- and y-axes are the sizes of metabolic (h) and replication (r) neighbourhood, respectively (N: von Neumann neighbourhood; 3: 3×3, 5: 5×5, 7: 7×7, 25: 25×25 and 37: 37×37 Moore neighbourhoods). The gray-scale shades of the boxes correspond to average replicator densities (%, see scale bar) on the whole grid at the end of the simulations (at t = 1.000). The numbers within the boxes of the panels indicate the average ratio (%) of the numbers of phenotype- and genotype forms at the end of the simulations (100 × Phenx/Genx, x = 1, .., 4) in five replicate runs of the simulation in each parameter set. Zero means the collapse of the system (no replicator survives to t = 1.000). Replication constants: k1p = 3.0, k1g = 4.0, k2p = 5.0, k2g = 6.0 , k3p = 7.0, k3g = 8.0, k4p = 9.0 and k4g = 10.0; subscripts p and g denote phenotype-forms and genotype-forms of replicator types, respectively.
Mentions: Wherever the system is persistent, its equilibrium state can be fully specified by the stationary densities of the replicator species, and the phenotype to genotype density ratio within each species. Figures 2 and 3 summarize these output data obtained with Model I to demonstrate the effect of gene/enzyme functional complementarity devoid of the replicability difference between the “enzyme” and the “gene” form of the same replicator type, without and with a parasite, respectively; Figures 4 and 5 show the same simulation outcomes for Model II. The data shown on the figures are the averages of five replicate simulations for each parameter setting.Figure 2

Bottom Line: The fact that RNA templates and their copies are of complementary base sequences has an obvious dynamical relevance: complementary strains may have very different structures and, consequently, functions - one may specialize for increasing enzymatic activity while the other takes the role of the gene of the enzyme.This asymmetry is expected to reverse due to the evolved trade-off of high "gene" replicability and high catalytic activity of the corresponding "enzyme" in expense of its replicability.This trade-off is the first evolutionary step towards the "division of labour" among enzymes and genes, which has concluded in the extreme form of phenotype amplification characteristic of our recent DNA-RNA-protein World.

View Article: PubMed Central - PubMed

ABSTRACT

Background: RNA or RNA-like polymers are the most likely candidates for having played the lead roles on the stage of the origin of life. RNA is known to feature two of the three essential functions of living entities (metabolism, heredity and membrane): it is capable of unlimited heredity and it has a proven capacity for catalysing very different chemical reactions which may form simple metabolic networks. The Metabolically Coupled Replicator System is a class of simulation models built on these two functions to show that an RNA World scenario for the origin of life is ecologically feasible, provided that it is played on mineral surfaces. The fact that RNA templates and their copies are of complementary base sequences has an obvious dynamical relevance: complementary strains may have very different structures and, consequently, functions - one may specialize for increasing enzymatic activity while the other takes the role of the gene of the enzyme.

Results: Incorporating the functional divergence of template and copy into the Metabolically Coupled Replicator System model framework we show that sequence complementarity 1) does not ruin the coexistence of a set of metabolically cooperating replicators; 2) the replicator system remains resistant to, but also tolerant with its parasites; 3) opens the way to the evolutionary differentiation of phenotype and genotype through a primitive version of phenotype amplification.

Conclusions: The functional asymmetry of complementary RNA strains results in a shift of phenotype/genotype (enzyme/gene) proportions in MCRS, favouring a slight genotype dominance. This asymmetry is expected to reverse due to the evolved trade-off of high "gene" replicability and high catalytic activity of the corresponding "enzyme" in expense of its replicability. This trade-off is the first evolutionary step towards the "division of labour" among enzymes and genes, which has concluded in the extreme form of phenotype amplification characteristic of our recent DNA-RNA-protein World.

Show MeSH
Related in: MedlinePlus