RESUMO
The standard genetic code defines the rules of translation for nearly every life form on Earth. It also determines the amino acid changes accessible via single-nucleotide mutations, thus influencing protein evolvability-the ability of mutation to bring forth adaptive variation in protein function. One of the most striking features of the standard genetic code is its robustness to mutation, yet it remains an open question whether such robustness facilitates or frustrates protein evolvability. To answer this question, we use data from massively parallel sequence-to-function assays to construct and analyze 6 empirical adaptive landscapes under hundreds of thousands of rewired genetic codes, including those of codon compression schemes relevant to protein engineering and synthetic biology. We find that robust genetic codes tend to enhance protein evolvability by rendering smooth adaptive landscapes with few peaks, which are readily accessible from throughout sequence space. However, the standard genetic code is rarely exceptional in this regard, because many alternative codes render smoother landscapes than the standard code. By constructing low-dimensional visualizations of these landscapes, which each comprise more than 16 million mRNA sequences, we show that such alternative codes radically alter the topological features of the network of high-fitness genotypes. Whereas the genetic codes that optimize evolvability depend to some extent on the detailed relationship between amino acid sequence and protein function, we also uncover general design principles for engineering nonstandard genetic codes for enhanced and diminished evolvability, which may facilitate directed protein evolution experiments and the bio-containment of synthetic organisms, respectively.
Assuntos
Evolução Molecular , Código Genético , Proteínas , Proteínas/genética , Proteínas/metabolismo , Mutação/genética , Códon/genética , Modelos Genéticos , Biologia Sintética/métodos , Biossíntese de Proteínas , Engenharia de Proteínas/métodosRESUMO
Evolvability is the ability of a biological system to produce phenotypic variation that is both heritable and adaptive. It has long been the subject of anecdotal observations and theoretical work. In recent years, however, the molecular causes of evolvability have been an increasing focus of experimental work. Here, we review recent experimental progress in areas as different as the evolution of drug resistance in cancer cells and the rewiring of transcriptional regulation circuits in vertebrates. This research reveals the importance of three major themes: multiple genetic and non-genetic mechanisms to generate phenotypic diversity, robustness in genetic systems, and adaptive landscape topography. We also discuss the mounting evidence that evolvability can evolve and the question of whether it evolves adaptively.
Assuntos
Resistencia a Medicamentos Antineoplásicos/genética , Evolução Molecular , Genótipo , Modelos Genéticos , Mutação , Neoplasias/genética , Animais , Simulação por Computador , Humanos , Neoplasias/metabolismoRESUMO
Evolutionary adaptation often occurs by the fixation of beneficial mutations. This mode of adaptation can be characterized quantitatively by a spectrum of adaptive substitutions, i.e., a distribution for types of changes fixed in adaptation. Recent work establishes that the changes involved in adaptation reflect common types of mutations, raising the question of how strongly the mutation spectrum shapes the spectrum of adaptive substitutions. We address this question with a codon-based model for the spectrum of adaptive amino acid substitutions, applied to three large datasets covering thousands of amino acid changes identified in natural and experimental adaptation in Saccharomyces cerevisiae, Escherichia coli, and Mycobacterium tuberculosis Using species-specific mutation spectra based on prior knowledge, we find that the mutation spectrum has a proportional influence on the spectrum of adaptive substitutions in all three species. Indeed, we find that by inferring the mutation rates that best explain the spectrum of adaptive substitutions, we can accurately recover the species-specific mutation spectra. However, we also find that the predictive power of the model differs substantially between the three species. To better understand these differences, we use population simulations to explore the factors that influence how closely the spectrum of adaptive substitutions mirrors the mutation spectrum. The results show that the influence of the mutation spectrum decreases with increasing mutational supply ([Formula: see text]) and that predictive power is strongly affected by the number and diversity of beneficial mutations.
Assuntos
Adaptação Fisiológica , Escherichia coli/genética , Mycobacterium tuberculosis/genética , Saccharomyces cerevisiae/genética , Proteínas de Bactérias/genética , Proteínas de Bactérias/metabolismo , Escherichia coli/fisiologia , Proteínas Fúngicas/genética , Proteínas Fúngicas/metabolismo , Regulação Bacteriana da Expressão Gênica , Regulação Fúngica da Expressão Gênica , Mutação , Mycobacterium tuberculosis/fisiologia , Saccharomyces cerevisiae/fisiologia , Especificidade da EspécieRESUMO
The notion that mutations are random relative to their fitness effects is central to the Neo-Darwinian view of evolution. However, a recent interpretation of the patterns of mutation accumulation in the genome of Arabidopsis thaliana has challenged this notion, arguing for the presence of a targeted DNA repair mechanism that causes a nonrandom association of mutation rates and fitness effects. Specifically, this mechanism was suggested to cause a reduction in the rates of mutations on essential genes, thus lowering the rates of deleterious mutations. Central to this argument were attempts to rule out selection at the population level. Here, we offer an alternative and parsimonious interpretation of the patterns of mutation accumulation previously attributed to mutation bias, showing how they can instead or additionally be caused by developmental selection, that is selection occurring at the cellular level during the development of a multicellular organism. Thus, the depletion of deleterious mutations in A. thaliana may indeed be the result of a selective process, rather than a bias in mutation. More broadly, our work highlights the importance of considering development in the interpretation of population-genetic analyses of multicellular organisms, and it emphasizes that efforts to identify mechanisms involved in mutational biases should explicitly account for developmental selection.
Assuntos
Genoma , Seleção Genética , Mutação , PercepçãoRESUMO
AbstractThe joint distribution of selection coefficients and mutation rates is a key determinant of the genetic architecture of molecular adaptation. Three different distributions are of immediate interest: (1) the "nominal" distribution of possible changes, prior to mutation or selection; (2) the "de novo" distribution of realized mutations; and (3) the "fixed" distribution of selectively established mutations. Here, we formally characterize the relationships between these joint distributions under the strong-selection/weak-mutation (SSWM) regime. The de novo distribution is enriched relative to the nominal distribution for the highest rate mutations, and the fixed distribution is further enriched for the most highly beneficial mutations. Whereas mutation rates and selection coefficients are often assumed to be uncorrelated, we show that even with no correlation in the nominal distribution, the resulting de novo and fixed distributions can have correlations with any combination of signs. Nonetheless, we suggest that natural systems with a finite number of beneficial mutations will frequently have the kind of nominal distribution that induces negative correlations in the fixed distribution. We apply our mathematical framework, along with population simulations, to explore joint distributions of selection coefficients and mutation rates from deep mutational scanning and cancer informatics. Finally, we consider the evolutionary implications of these joint distributions together with two additional joint distributions relevant to parallelism and the rate of adaptation.
Assuntos
Taxa de Mutação , Seleção Genética , Modelos Genéticos , Mutação , Evolução Biológica , Evolução MolecularRESUMO
The mapping from genotype to phenotype to fitness typically involves multiple nonlinearities that can transform the effects of mutations. For example, mutations may contribute additively to a phenotype, but their effects on fitness may combine non-additively because selection favors a low or intermediate value of that phenotype. This can cause incongruence between the topographical properties of a fitness landscape and its underlying genotype-phenotype landscape. Yet, genotype-phenotype landscapes are often used as a proxy for fitness landscapes to study the dynamics and predictability of evolution. Here, we use theoretical models and empirical data on transcription factor-DNA interactions to systematically study the incongruence of genotype-phenotype and fitness landscapes when selection favors a low or intermediate phenotypic value. Using the theoretical models, we prove a number of fundamental results. For example, selection for low or intermediate phenotypic values does not change simple sign epistasis into reciprocal sign epistasis, implying that genotype-phenotype landscapes with only simple sign epistasis motifs will always give rise to single-peaked fitness landscapes under such selection. More broadly, we show that such selection tends to create fitness landscapes that are more rugged than the underlying genotype-phenotype landscape, but this increased ruggedness typically does not frustrate adaptive evolution because the local adaptive peaks in the fitness landscape tend to be nearly as tall as the global peak. Many of these results carry forward to the empirical genotype-phenotype landscapes, which may help to explain why low- and intermediate-affinity transcription factor-DNA interactions are so prevalent in eukaryotic gene regulation.
Assuntos
Epistasia Genética , Modelos Genéticos , Epistasia Genética/genética , Aptidão Genética/genética , Genótipo , Mutação/genética , Fenótipo , Fatores de TranscriçãoRESUMO
Selection for resource conservation can shape the coding sequences of organisms living in nutrient-limited environments. Recently, it was proposed that selection for resource conservation, specifically for nitrogen and carbon content, has also shaped the structure of the standard genetic code, such that the missense mutations the code allows tend to cause small increases in the number of nitrogen and carbon atoms in amino acids. Moreover, it was proposed that this optimization is not confounded by known optimizations of the standard genetic code, such as for polar requirement or hydropathy. We challenge these claims. We show the proposed optimization for nitrogen conservation is highly sensitive to choice of null model and the proposed optimization for carbon conservation is confounded by the known conservative nature of the standard genetic code with respect to the molecular volume of amino acids. There is therefore little evidence the standard genetic code is optimized for resource conservation. We discuss our findings in the context of null models of the standard genetic code.
Assuntos
Evolução Molecular , Código Genético , Aminoácidos/genética , Modelos Genéticos , Mutação de Sentido Incorreto , NitrogênioRESUMO
AbstractThe adaptive potential of nonheritable somatic mutations has received limited attention in traditional evolutionary theory because heritability is a fundamental pillar of Darwinian evolution. We hypothesized that the ability of a germline genotype to express a novel phenotype via nonheritable somatic mutations can be selectively advantageous and that this advantage will channel evolving populations toward germline genotypes that constitutively express the phenotype. We tested this hypothesis by simulating evolving populations of developing organisms with an impermeable germline-soma separation navigating a minimal fitness landscape. The simulations revealed the conditions under which nonheritable somatic mutations promote adaptation. Specifically, this can occur when the somatic mutation supply is high, when few cells with the advantageous somatic mutation are required to increase organismal fitness, and when the somatic mutation also confers a selective advantage at the cellular level. We therefore provide proof of principle that nonheritable somatic mutations can promote adaptive evolution via a process we call "somatic genotypic exploration." We discuss the biological plausibility of this phenomenon as well as its evolutionary implications.
Assuntos
Adaptação Fisiológica , Células Germinativas , Genótipo , Adaptação Fisiológica/genética , Aclimatação , MutaçãoRESUMO
Transition bias, an overabundance of transitions relative to transversions, has been widely reported among studies of the rates and spectra of spontaneous mutations. However, demonstrating the role of transition bias in adaptive evolution remains challenging. In particular, it is unclear whether such biases direct the evolution of bacterial pathogens adapting to treatment. We addressed this challenge by analyzing adaptive antibiotic-resistance mutations in the major human pathogen Mycobacterium tuberculosis (MTB). We found strong evidence for transition bias in two independently curated data sets comprising 152 and 208 antibiotic-resistance mutations. This was true at the level of mutational paths (distinct adaptive DNA sequence changes) and events (individual instances of the adaptive DNA sequence changes) and across different genes and gene promoters conferring resistance to a diversity of antibiotics. It was also true for mutations that do not code for amino acid changes (in gene promoters and the 16S ribosomal RNA gene rrs) and for mutations that are synonymous to each other and are therefore likely to have similar fitness effects, suggesting that transition bias can be caused by a bias in mutation supply. These results point to a central role for transition bias in determining which mutations drive adaptive antibiotic resistance evolution in a key pathogen.
Assuntos
Farmacorresistência Bacteriana/genética , Evolução Molecular , Mycobacterium tuberculosis/genética , Sequência de Aminoácidos , Proteínas de Bactérias/química , Proteínas de Bactérias/genética , Mutação/genética , Nucleotídeos/genética , FilogeniaRESUMO
Regulatory networks control the spatiotemporal gene expression patterns that give rise to and define the individual cell types of multicellular organisms. In eumetazoa, distal regulatory elements called enhancers play a key role in determining the structure of such networks, particularly the wiring diagram of "who regulates whom." Mutations that affect enhancer activity can therefore rewire regulatory networks, potentially causing adaptive changes in gene expression. Here, we use whole-tissue and single-cell transcriptomic and chromatin accessibility data from mouse to show that enhancers play an additional role in the evolution of regulatory networks: They facilitate network growth by creating transcriptionally active regions of open chromatin that are conducive to de novo gene evolution. Specifically, our comparative transcriptomic analysis with three other mammalian species shows that young, mouse-specific intergenic open reading frames are preferentially located near enhancers, whereas older open reading frames are not. Mouse-specific intergenic open reading frames that are proximal to enhancers are more highly and stably transcribed than those that are not proximal to enhancers or promoters, and they are transcribed in a limited diversity of cellular contexts. Furthermore, we report several instances of mouse-specific intergenic open reading frames proximal to promoters showing evidence of being repurposed enhancers. We also show that open reading frames gradually acquire interactions with enhancers over macroevolutionary timescales, helping integrate genes-those that have arisen de novo or by other means-into existing regulatory networks. Taken together, our results highlight a dual role of enhancers in expanding and rewiring gene regulatory networks.
Assuntos
Elementos Facilitadores Genéticos , Evolução Molecular , Redes Reguladoras de Genes , Animais , DNA Intergênico , Camundongos , Fases de Leitura Aberta , Regiões Promotoras Genéticas , Transcrição GênicaRESUMO
Mutation is a biased stochastic process, with some types of mutations occurring more frequently than others. Previous work has used synthetic genotype-phenotype landscapes to study how such mutation bias affects adaptive evolution. Here, we consider 746 empirical genotype-phenotype landscapes, each of which describes the binding affinity of target DNA sequences to a transcription factor, to study the influence of mutation bias on adaptive evolution of increased binding affinity. By using empirical genotype-phenotype landscapes, we need to make only few assumptions about landscape topography and about the DNA sequences that each landscape contains. The latter is particularly important because the set of sequences that a landscape contains determines the types of mutations that can occur along a mutational path to an adaptive peak. That is, landscapes can exhibit a composition bias-a statistical enrichment of a particular type of mutation relative to a null expectation, throughout an entire landscape or along particular mutational paths-that is independent of any bias in the mutation process. Our results reveal the way in which composition bias interacts with biases in the mutation process under different population genetic conditions, and how such interaction impacts fundamental properties of adaptive evolution, such as its predictability, as well as the evolution of genetic diversity and mutational robustness.
Assuntos
Evolução Molecular , Modelos Genéticos , Mutação , Biologia Computacional , DNA Bacteriano/química , DNA Bacteriano/genética , DNA Bacteriano/metabolismo , Genótipo , Mutação/genética , Mutação/fisiologia , Fenótipo , Ligação Proteica/genética , Fatores de Transcrição/química , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismoRESUMO
Much of gene regulation is carried out by proteins that bind DNA or RNA molecules at specific sequences. One class of such proteins is transcription factors, which bind short DNA sequences to regulate transcription. Another class is RNA binding proteins, which bind short RNA sequences to regulate RNA maturation, transport, and stability. Here, we study the robustness and evolvability of these regulatory mechanisms. To this end, we use experimental binding data from 172 human and fruit fly transcription factors and RNA binding proteins as well as human polymorphism data to study the evolution of binding sites in vivo. We find little difference between the robustness of regulatory protein-RNA interactions and transcription factor-DNA interactions to DNA mutations. In contrast, we find that RNA-mediated regulation is less evolvable than transcriptional regulation, because mutations are less likely to create interactions of an RNA molecule with a new RNA binding protein than they are to create interactions of a gene regulatory region with a new transcription factor. Our observations are consistent with the high level of conservation observed for interactions between RNA binding proteins and their target molecules as well as the evolutionary plasticity of regulatory regions bound by transcription factors. They may help explain why transcriptional regulation is implicated in many more evolutionary adaptations and innovations than RNA-mediated gene regulation.
Assuntos
Regulação da Expressão Gênica/genética , Processamento Pós-Transcricional do RNA/genética , Fatores de Transcrição/genética , Animais , Sítios de Ligação/genética , DNA/metabolismo , Proteínas de Ligação a DNA/metabolismo , Drosophila/genética , Evolução Molecular , Regulação da Expressão Gênica/fisiologia , Humanos , Mutação , RNA/metabolismo , Proteínas de Ligação a RNA/metabolismo , Sequências Reguladoras de Ácido Nucleico , Fatores de Transcrição/metabolismo , Transcrição Gênica/genéticaRESUMO
A genotype network is a graph in which vertices represent genotypes that have the same phenotype. Edges connect vertices if their corresponding genotypes differ in a single small mutation. Genotype networks are used to study the organization of genotype spaces. They have shed light on the relationship between robustness and evolvability in biological systems as different as RNA macromolecules and transcriptional regulatory circuits. Despite the importance of genotype networks, no tool exists for their automatic construction, analysis and visualization. Here we fill this gap by presenting the Genonets Server, a tool that provides the following features: (i) the construction of genotype networks for categorical and univariate phenotypes from DNA, RNA, amino acid or binary sequences; (ii) analyses of genotype network topology and how it relates to robustness and evolvability, as well as analyses of genotype network topography and how it relates to the navigability of a genotype network via mutation and natural selection; (iii) multiple interactive visualizations that facilitate exploratory research and education. The Genonets Server is freely available at http://ieu-genonets.uzh.ch.
Assuntos
Redes Reguladoras de Genes , Genótipo , Fenótipo , Interface Usuário-Computador , Sequência de Aminoácidos , Gráficos por Computador , DNA/genética , Evolução Molecular , Regulação da Expressão Gênica , Humanos , Internet , Mutação , RNA/genética , Seleção Genética , Vírus/genéticaRESUMO
Many developmental, physiological, and behavioral processes depend on the precise expression of genes in space and time. Such spatiotemporal gene expression phenotypes arise from the binding of sequence-specific transcription factors (TFs) to DNA, and from the regulation of nearby genes that such binding causes. These nearby genes may themselves encode TFs, giving rise to a transcription factor network (TFN), wherein nodes represent TFs and directed edges denote regulatory interactions between TFs. Computational studies have linked several topological properties of TFNs - such as their degree distribution - with the robustness of a TFN's gene expression phenotype to genetic and environmental perturbation. Another important topological property is assortativity, which measures the tendency of nodes with similar numbers of edges to connect. In directed networks, assortativity comprises four distinct components that collectively form an assortativity signature. We know very little about how a TFN's assortativity signature affects the robustness of its gene expression phenotype to perturbation. While recent theoretical results suggest that increasing one specific component of a TFN's assortativity signature leads to increased phenotypic robustness, the biological context of this finding is currently limited because the assortativity signatures of real-world TFNs have not been characterized. It is therefore unclear whether these earlier theoretical findings are biologically relevant. Moreover, it is not known how the other three components of the assortativity signature contribute to the phenotypic robustness of TFNs. Here, we use publicly available DNaseI-seq data to measure the assortativity signatures of genome-wide TFNs in 41 distinct human cell and tissue types. We find that all TFNs share a common assortativity signature and that this signature confers phenotypic robustness to model TFNs. Lastly, we determine the extent to which each of the four components of the assortativity signature contributes to this robustness.
Assuntos
Redes Reguladoras de Genes/genética , Modelos Genéticos , Fenótipo , Fatores de Transcrição/genética , Biologia Computacional , Regulação da Expressão Gênica/genética , Humanos , Especificidade de Órgãos , Fatores de Transcrição/química , Fatores de Transcrição/metabolismoRESUMO
Gene regulatory circuits drive the development, physiology, and behavior of organisms from bacteria to humans. The phenotypes or functions of such circuits are embodied in the gene expression patterns they form. Regulatory circuits are typically multifunctional, forming distinct gene expression patterns in different embryonic stages, tissues, or physiological states. Any one circuit with a single function can be realized by many different regulatory genotypes. Multifunctionality presumably constrains this number, but we do not know to what extent. We here exhaustively characterize a genotype space harboring millions of model regulatory circuits and all their possible functions. As a circuit's number of functions increases, the number of genotypes with a given number of functions decreases exponentially but can remain very large for a modest number of functions. However, the sets of circuits that can form any one set of functions becomes increasingly fragmented. As a result, historical contingency becomes widespread in circuits with many functions. Whether a circuit can acquire an additional function in the course of its evolution becomes increasingly dependent on the function it already has. Circuits with many functions also become increasingly brittle and sensitive to mutation. These observations are generic properties of a broad class of circuits and independent of any one circuit genotype or phenotype.
Assuntos
Redes Reguladoras de Genes , Modelos Genéticos , Expressão Gênica , Genótipo , HumanosRESUMO
Gene regulatory networks (GRNs) represent the interactions between genes and gene products, which drive the gene expression patterns that produce cellular phenotypes. GRNs display a number of characteristics that are beneficial for the development and evolution of organisms. For example, they are often robust to genetic perturbation, such as mutations in regulatory regions or loss of gene function. Simultaneously, GRNs are often evolvable as these genetic perturbations are occasionally exploited to innovate novel regulatory programs. Several topological properties, such as degree distribution, are known to influence the robustness and evolvability of GRNs. Assortativity, which measures the propensity of nodes of similar connectivity to connect to one another, is a separate topological property that has recently been shown to influence the robustness of GRNs to point mutations in cis-regulatory regions. However, it remains to be seen how assortativity may influence the robustness and evolvability of GRNs to other forms of genetic perturbation, such as gene birth via duplication or de novo origination. Here, we employ a computational model of genetic regulation to investigate whether the assortativity of a GRN influences its robustness and evolvability upon gene birth. We find that the robustness of a GRN generally increases with increasing assortativity, while its evolvability generally decreases. However, the rate of change in robustness outpaces that of evolvability, resulting in an increased proportion of assortative GRNs that are simultaneously robust and evolvable. By providing a mechanistic explanation for these observations, this work extends our understanding of how the assortativity of a GRN influences its robustness and evolvability upon gene birth.
Assuntos
Evolução Molecular , Regulação da Expressão Gênica/fisiologia , Modelos Biológicos , Elementos Reguladores de Transcrição/fisiologia , Mutação PuntualRESUMO
Mutations to gene regulatory networks can be maladaptive or a source of evolutionary novelty. Epistasis confounds our understanding of how mutations affect the expression patterns of gene regulatory networks, a challenge exacerbated by the dependence of epistasis on the environment. We used the toolkit of synthetic biology to systematically assay the effects of pairwise and triplet combinations of mutant genotypes on the expression pattern of a gene regulatory network expressed in Escherichia coli that interprets an inducer gradient across a spatial domain. We uncovered a preponderance of epistasis that can switch in magnitude and sign across the inducer gradient to produce a greater diversity of expression pattern phenotypes than would be possible in the absence of such environment-dependent epistasis. We discuss our findings in the context of the evolution of hybrid incompatibilities and evolutionary novelties.
Assuntos
Epistasia Genética , Redes Reguladoras de Genes , Fenótipo , Genótipo , Bioensaio , Escherichia coli/genéticaRESUMO
Predicting evolutionary outcomes is an important research goal in a diversity of contexts. The focus of evolutionary forecasting is usually on adaptive processes, and efforts to improve prediction typically focus on selection. However, adaptive processes often rely on new mutations, which can be strongly influenced by predictable biases in mutation. Here, we provide an overview of existing theory and evidence for such mutation-biased adaptation and consider the implications of these results for the problem of prediction, in regard to topics such as the evolution of infectious diseases, resistance to biochemical agents, as well as cancer and other kinds of somatic evolution. We argue that empirical knowledge of mutational biases is likely to improve in the near future, and that this knowledge is readily applicable to the challenges of short-term prediction. This article is part of the theme issue 'Interdisciplinary approaches to predicting evolutionary biology'.
Assuntos
Adaptação Fisiológica , Evolução Biológica , Mutação , Adaptação Fisiológica/genética , Aclimatação , Viés , Evolução MolecularRESUMO
Gene regulatory networks (GRNs) drive the cellular processes that sustain life. To do so reliably, GRNs must be robust to perturbations, such as gene deletion and the addition or removal of regulatory interactions. GRNs must also be robust to genetic changes in regulatory regions that define the logic of signal-integration, as these changes can affect how specific combinations of regulatory signals are mapped to particular gene expression states. Previous theoretical analyses have demonstrated that the robustness of a GRN is influenced by its underlying topological properties, such as degree distribution and modularity. Another important topological property is assortativity, which measures the propensity with which nodes of similar connectivity are connected to one another. How assortativity influences the robustness of the signal-integration logic of GRNs remains an open question. Here, we use computational models of GRNs to investigate this relationship. We separately consider each of the three dynamical regimes of this model for a variety of degree distributions. We find that in the chaotic regime, robustness exhibits a pronounced increase as assortativity becomes more positive, while in the critical and ordered regimes, robustness is generally less sensitive to changes in assortativity. We attribute the increased robustness to a decrease in the duration of the gene expression pattern, which is caused by a reduction in the average size of a GRN's in-components. This study provides the first direct evidence that assortativity influences the robustness of the signal-integration logic of computational models of GRNs, illuminates a mechanistic explanation for this influence, and furthers our understanding of the relationship between topology and robustness in complex biological systems.
Assuntos
Redes Reguladoras de Genes/fisiologia , Modelos Genéticos , Animais , Simulação por Computador , Genótipo , Fenótipo , Transdução de Sinais/genéticaRESUMO
Dispersal modulates gene flow throughout a population's spatial range. Gene flow affects adaptation at local spatial scales, and consequently impacts the evolution of reproductive isolation. A recent theoretical investigation has demonstrated that local adaptation along an environmental gradient, facilitated by the evolution of limited dispersal, can lead to parapatric speciation even in the absence of assortative mating. This and other studies assumed unconditional dispersal, so individuals start dispersing without regard to local environmental conditions. However, many species disperse conditionally; their propensity to disperse is contingent upon environmental cues, such as the degree of local crowding or the availability of suitable mates. Here, we use an individual-based model in continuous space to investigate by numerical simulation the relationship between the evolution of threshold-based conditional dispersal and parapatric speciation driven by frequency-dependent competition along environmental gradients. We find that, as with unconditional dispersal, parapatric speciation occurs under a broad range of conditions when reproduction is asexual, and under a more restricted range of conditions when reproduction is sexual. In both the asexual and sexual cases, the evolution of conditional dispersal is strongly influenced by the slope of the environmental gradient: shallow environmental gradients result in low dispersal thresholds and high dispersal distances, while steep environmental gradients result in high dispersal thresholds and low dispersal distances. The latter, however, remain higher than under unconditional dispersal, thus undermining isolation by distance, and hindering speciation in sexual populations. Consequently, the speciation of sexual populations under conditional dispersal is triggered by a steeper gradient than under unconditional dispersal. Enhancing the disruptiveness of frequency-dependent selection, more box-shaped competition kernels dramatically lower the speciation-enabling slope of the environmental gradient.