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PubMed2006

The evolution of the histone methyltransferase gene Su(var)3-9 in metazoans includes a fusion with and a re-fission from a functionally unrelated gene.

BACKGROUND: In eukaryotes, histone H3 lysine 9 (H3K9) methylation is a common mechanism involved in gene silencing and the establishment of heterochromatin. The loci of the major heterochromatic H3K9 methyltransferase Su(var)3-9 and the functionally unrelated gamma subunit of the translation initiation factor eIF2 are fused in Drosophila melanogaster. Here we examined the phylogenetic distribution of this unusual gene fusion and the molecular evolution of the H3K9 HMTase Su(var)3-9. RESULTS: We show that the gene fusion had taken place in the ancestral line of winged insects and silverfishs (Dicondylia) about 400 million years ago. We cloned Su(var)3-9 genes from a collembolan and a spider where both genes ancestrally exist as independent transcription units. In contrast, we found a Su(var)3-9-specific exon inside the conserved intron position 81-1 of the eIF2gamma gene structure in species of eight different insect orders. Intriguinly, in the pea aphid Acyrthosiphon pisum, we detected only sequence remains of this Su(var)3-9 exon in the eIF2gamma intron, along with an eIF2gamma-independent Su(var)3-9 gene. This reveals an evolutionary re-fission of both genes in aphids. Su(var)3-9 chromo domains are similar to HP1 chromo domains, which points to a potential binding activity to methylated K9 of histone H3. SET domain comparisons suggest a weaker methyltransferase activity of Su(var)3-9 in comparison to other H3K9 HMTases. Astonishingly, 11 of 19 previously described, deleterious amino acid substitutions found in Drosophila Su(var)3-9 are seemingly compensable through accompanying substitutions during evolution. CONCLUSION: Examination of the Su(var)3-9 evolution revealed strong evidence for the establishment of the Su(var)3-9/eIF2gamma gene fusion in an ancestor of dicondylic insects and a re-fission of this fusion during the evolution of aphids. Our comparison of 65 selected chromo domains and 93 selected SET domains from Su(var)3-9 and related proteins offers functional predictions concerning both domains in Su(var)3-9 proteins.

Amino Acid Sequence↗

PubMed2004

Molecular clock in neutral protein evolution.

BACKGROUND: A frequent observation in molecular evolution is that amino-acid substitution rates show an index of dispersion (that is, ratio of variance to mean) substantially larger than one. This observation has been termed the overdispersed molecular clock. On the basis of in silico protein-evolution experiments, Bastolla and coworkers recently proposed an explanation for this observation: Proteins drift in neutral space, and can temporarily get trapped in regions of substantially reduced neutrality. In these regions, substitution rates are suppressed, which results in an overall substitution process that is not Poissonian. However, the simulation method of Bastolla et al. is representative only for cases in which the product of mutation rate micro and population size Ne is small. How the substitution process behaves when micro Ne is large is not known. RESULTS: Here, I study the behavior of the molecular clock in in silico protein evolution as a function of mutation rate and population size. I find that the index of dispersion decays with increasing micro Ne, and approaches 1 for large micro Ne. This observation can be explained with the selective pressure for mutational robustness, which is effective when micro Ne is large. This pressure keeps the population out of low-neutrality traps, and thus steadies the ticking of the molecular clock. CONCLUSIONS: The molecular clock in neutral protein evolution can fall into two distinct regimes, a strongly overdispersed one for small micro Ne, and a mostly Poissonian one for large micro Ne. The former is relevant for the majority of organisms in the plant and animal kingdom, and the latter may be relevant for RNA viruses.

Amino Acid Substitution↗

PubMed2006

Fast rate of evolution in alternatively spliced coding regions of mammalian genes.

BACKGROUND: At least half of mammalian genes are alternatively spliced. Alternative isoforms are often genome-specific and it has been suggested that alternative splicing is one of the major mechanisms for generating protein diversity in the course of evolution. Another way of looking at alternative splicing is to consider sequence evolution of constitutive and alternative regions of protein-coding genes. Indeed, it turns out that constitutive and alternative regions evolve in different ways. RESULTS: A set of 3029 orthologous pairs of human and mouse alternatively spliced genes was considered. The rate of nonsynonymous substitutions (dN), the rate of synonymous substitutions (dS), and their ratio (omega = dN/dS) appear to be significantly higher in alternatively spliced coding regions compared to constitutive regions. When N-terminal, internal and C-terminal alternatives are analysed separately, C-terminal alternatives appear to make the main contribution to the observed difference. The effects become even more pronounced in a subset of fast evolving genes. CONCLUSION: These results provide evidence of weaker purifying selection and/or stronger positive selection in alternative regions and thus one more confirmation of accelerated evolution in alternative regions. This study corroborates the theory that alternative splicing serves as a testing ground for molecular evolution.

Alternative Splicing↗

PubMed2006

Adaptive evolution of the spike gene of SARS coronavirus: changes in positively selected sites in different epidemic groups.

BACKGROUND: It is believed that animal-to-human transmission of severe acute respiratory syndrome (SARS) coronavirus (CoV) is the cause of the SARS outbreak worldwide. The spike (S) protein is one of the best characterized proteins of SARS-CoV, which plays a key role in SARS-CoV overcoming species barrier and accomplishing interspecies transmission from animals to humans, suggesting that it may be the major target of selective pressure. However, the process of adaptive evolution of S protein and the exact positively selected sites associated with this process remain unknown. RESULTS: By investigating the adaptive evolution of S protein, we identified twelve amino acid sites (75, 239, 244, 311, 479, 609, 613, 743, 765, 778, 1148, and 1163) in the S protein under positive selective pressure. Based on phylogenetic tree and epidemiological investigation, SARS outbreak was divided into three epidemic groups: 02-04 interspecies, 03-early-mid, and 03-late epidemic groups in the present study. Positive selection was detected in the first two groups, which represent the course of SARS-CoV interspecies transmission and of viral adaptation to human host, respectively. In contrast, purifying selection was detected in 03-late group. These indicate that S protein experiences variable positive selective pressures before reaching stabilization. A total of 25 sites in 02-04 interspecies epidemic group and 16 sites in 03-early-mid epidemic group were identified under positive selection. The identified sites were different between these two groups except for site 239, which suggests that positively selected sites are changeable between groups. Moreover, it was showed that a larger proportion (24%) of positively selected sites was located in receptor-binding domain (RBD) than in heptad repeat (HR)1-HR2 region in 02-04 interspecies epidemic group (p = 0.0208), and a greater percentage (25%) of these sites occurred in HR1-HR2 region than in RBD in 03-early-mid epidemic group (p = 0.0721). These suggest that functionally different domains of S protein may not experience same positive selection in each epidemic group. In addition, three specific replacements (F360S, T487S and L665S) were only found between 03-human SARS-CoVs and strains from 02-04 interspecies epidemic group, which reveals that selective sweep may also force the evolution of S genes before the jump of SARS-CoVs into human hosts. Since certain residues at these positively selected sites are associated with receptor recognition and/or membrane fusion, they are likely to be the crucial residues for animal-to-human transmission of SARS-CoVs, and subsequent adaptation to human hosts. CONCLUSION: The variation of positive selective pressures and positively selected sites are likely to contribute to the adaptive evolution of S protein from animals to humans.

Amino Acid Sequence↗

PubMed2005

Divergence, recombination and retention of functionality during protein evolution.

We have only a vague idea of precisely how protein sequences evolve in the context of protein structure and function. This is primarily because structural and functional contexts are not easily predictable from the primary sequence, and evaluating patterns of evolution at individual residue positions is also difficult. As a result of increasing biodiversity in genomics studies, progress is being made in detecting context-dependent variation in substitution processes, but it remains unclear exactly what context-dependent patterns we should be looking for. To address this, we have been simulating protein evolution in the context of structure and function using lattice models of proteins and ligands (or substrates). These simulations include thermodynamic features of protein stability and population dynamics. We refer to this approach as 'ab initio evolution' to emphasise the fact that the equilibrium details of fitness distributions arise from the physical principles of the system and not from any preconceived notions or arbitrary mathematical distributions. Here, we present results on the retention of functionality in homologous recombinants following population divergence. A central result is that protein structure characteristics can strongly influence recombinant functionality. Exceptional structures with many sequence options evolve quickly and tend to retain functionality--even in highly diverged recombinants. By contrast, the more common structures with fewer sequence options evolve more slowly, but the fitness of recombinants drops off rapidly as homologous proteins diverge. These results have implications for understanding viral evolution, speciation and directed evolutionary experiments. Our analysis of the divergence process can also guide improved methods for accurately approximating folding probabilities in more complex but realistic systems.

Evolution, Molecular↗

PubMed2004

Evolution of the HIV-1 envelope glycoproteins with a disulfide bond between gp120 and gp41.

BACKGROUND: We previously described the construction of an HIV-1 envelope glycoprotein complex (Env) that is stabilized by an engineered intermolecular disulfide bond (SOS) between gp120 and gp41. The modified Env protein antigenically mimics the functional wild-type Env complex. Here, we explore the effects of the covalent gp120 - gp41 interaction on virus replication and evolution. RESULTS: An HIV-1 molecular clone containing the SOS Env gene was only minimally replication competent, suggesting that the engineered disulfide bond substantially impaired Env function. However, virus evolution occurred in cell culture infections, and it eventually always led to elimination of the intermolecular disulfide bond. In the course of these evolution studies, we identified additional and unusual second-site reversions within gp41. CONCLUSIONS: These evolution paths highlight residues that play an important role in the interaction between gp120 and gp41. Furthermore, our results suggest that a covalent gp120 - gp41 interaction is incompatible with HIV-1 Env function, probably because this impedes conformational changes that are necessary for fusion to occur, which may involve the complete dissociation of gp120 from gp41.

Amino Acid Substitution↗

PubMed2003

Genesis and evolution of the Evx and Mox genes and the extended Hox and ParaHox gene clusters.

BACKGROUND: Hox and ParaHox gene clusters are thought to have resulted from the duplication of a ProtoHox gene cluster early in metazoan evolution. However, the origin and evolution of the other genes belonging to the extended Hox group of homeobox-containing genes, that is, Mox and Evx, remains obscure. We constructed phylogenetic trees with mouse, amphioxus and Drosophila extended Hox and other related Antennapedia-type homeobox gene sequences and analyzed the linkage data available for such genes. RESULTS: We claim that neither Mox nor Evx is a Hox or ParaHox gene. We propose a scenario that reconciles phylogeny with linkage data, in which an Evx/Mox ancestor gene linked to a ProtoHox cluster was involved in a segmental tandem duplication event that generated an array of all Hox-like genes, referred to as the 'coupled' cluster. A chromosomal breakage within this cluster explains the current composition of the extended Hox cluster (with Evx, Hox and Mox genes) and the ParaHox cluster. CONCLUSIONS: Most studies dealing with the origin and evolution of Hox and ParaHox clusters have not included the Hox-related genes Mox and Evx. Our phylogenetic analyses and the available linkage data in mammalian genomes support an evolutionary scenario in which an ancestor of Evx and Mox was linked to the ProtoHox cluster, and that a tandem duplication of a large genomic region early in metazoan evolution generated the Hox and ParaHox clusters, plus the cluster-neighbors Evx and Mox. The large 'coupled' Hox-like cluster EvxHox/MoxParaHox was subsequently broken, thus grouping the Mox and Evx genes to the Hox clusters, and isolating the ParaHox cluster.

Animals↗

PubMed2006

Co-evolution of transcription factors and their targets depends on mode of regulation.

BACKGROUND: Differences in the transcription regulation network are at the root of much of the phenotypic variation observed among organisms. These differences may be achieved either by changing the repertoire of regulators and/or their targets, or by rewiring the network. Following these changes and studying their logic is crucial for understanding the evolution of regulatory networks. RESULTS: We use the well characterized transcription regulatory network of Escherichia coli K12 and follow the evolutionary changes in the repertoire of regulators and their targets across a large number of fully sequenced gamma-proteobacteria. By focusing on close relatives of E. coli K12, we study the dynamics of the evolution of transcription regulation across a relatively short evolutionary timescale. We show significant differences in the evolution of repressors and activators. Repressors are only lost from a genome once their targets have themselves been lost, or once the network has significantly rewired. In contrast, activators are often lost even when their targets remain in the genome. As a result, E. coli K12 repressors that regulate many targets are rarely absent from organisms that are closely related to E. coli K12, while activators with a similar number of targets are often absent in these organisms. CONCLUSION: We demonstrate that the mode of regulation exerted by transcription factors has a strong effect on their evolution. Repressors co-evolve tightly with their target genes. In contrast, activators can be lost independently of their targets. In fact, loss of an activator can lead to efficient shutdown of an unnecessary pathway.

Escherichia coli↗

PubMed2005

Evolution of the signaling system in relaxin-family peptides.

Recent studies have characterized two G-protein-coupled receptors (GPCRs), LGR7 and LGR8, as relaxin receptors. Later studies have shown that LGR7 and LGR8 also are cognate receptors for the relaxin-family peptides, INSL7/relaxin3 and INSL3, respectively. In addition, INSL7/relaxin3 signals through two orphan GPCRs, GPCR135 and GPCR142, whereas INSL5 is a select ligand for GPCR142. These findings have greatly enhanced our understanding of the physiology and signaling of this unique group of peptide hormones. Phylogenetic analysis of relaxin-family peptides and their co-evolved receptors suggests that the ancestor relaxin gene duplicated multiple times in a vertebrate branch-specific manner. Among the seven human relaxin-family peptides (relaxin1, relaxin2, INSL3/RLF, INSL4/EPIL, INSL5/RIF2, INSL6/RIF1, and INSL7/relaxin3), INSL7 and INSL5 could represent the most ancient form. By contrast, the most widely studied family peptides, human relaxins H1 and H2, appear to be derived from recent gene duplication in mammals. Therefore, relaxin-family peptides could be important for the evolution and adaptation to lineage-specific physiologic processes during evolution. Duplicated relaxin-family genes assumed regulatory roles in newly evolved reproductive processes, and relaxin/LGR signaling was harnessed for signaling in the uterus and mammary gland in addition to other tissues. Although the precise evolutionary history of relaxin ligand/receptor pairs remains to be elucidated, these findings indicate that the expansion of relaxin-family genes and their specific regulatory functions have evolved during vertebrate evolution to allow the development of a tissue-specific regulatory mechanism in a lineage-specific manner and provide a revealing portrait of molecular evolution in action.

Animals↗

PubMed2005

Allometric scaling of flight energetics in orchid bees: evolution of flux capacities and flux rates.

The evolution of metabolic pathways involved in energy production was studied in the flight muscles of 28 species of orchid bees. Previous work revealed that wingbeat frequencies and mass-specific metabolic rates decline in parallel by threefold as body mass increases interspecifically over a 20-fold range. We investigated the correlated evolution of metabolic rates during hovering flight and the flux capacities, i.e. V(max) values, of flight muscle enzymes involved in substrate catabolism, the Krebs cycle and the electron transport chain. V(max) at the hexokinase (HK) step scales allometrically with an exponent almost identical to those obtained for wingbeat frequency and mass-specific metabolic rate. Analysis of this relationship using phylogenetically independent contrasts supports the hypothesis of correlated evolution between HK activity and mass-specific metabolic rate. Although other enzymes scale allometrically with respect to body mass, e.g. trehalase, glycogen phosphorylase and citrate synthase, no other enzyme activities were correlated with metabolic rate after controlling for phylogenetic relatedness. Pathway flux rates were used with enzyme V(max) values to estimate fractional velocities (fraction of V(max) at which enzymes operate) for various reactions to gain insights into enzyme function and how this varies with body mass. Fractional velocity is highly conserved across species at the HK step, but varied at all other steps examined. These results are discussed in the context of the regulation and evolution of pathways of energy metabolism.

Animals↗

PubMed1992

Evolution and isoforms of V-ATPase subunits.

The structure of V- and F-ATPases/ATP synthases is remarkably conserved throughout evolution. Sequence analyses show that the V- and F-ATPases evolved from the same enzyme that was already present in the last common ancestor of all known extant life forms. The catalytic and non-catalytic subunits found in the dissociable head groups of both V-ATPases and F-ATPases are paralogous subunits, i.e. these two types of subunits evolved from a common ancestral gene. The gene duplication giving rise to these two genes (i.e. those encoding the catalytic and non-catalytic subunits) pre-dates the time of the last common ancestor. Similarities between the V- and F-ATPase subunits and an ATPase-like protein that is implicated in flagellar assembly are evaluated with regard to the early evolution of ATPases. Mapping of gene duplication events that occurred in the evolution of the proteolipid, the non-catalytic and the catalytic subunits onto the tree of life leads to a prediction of the likely quaternary structure of the encoded ATPases. The phylogenetic implications of V-ATPases found in eubacteria are discussed. Different V-ATPase isoforms have been detected in some higher eukaryotes, whereas others were shown to have only a single gene encoding the catalytic V-ATPase subunit. These data are analyzed with respect to the possible function of the different isoforms (tissue-specific, organelle-specific). The point in evolution at which the different isoforms arose is mapped by phylogenetic analysis.

Adenosine Triphosphatases↗

PubMed1998

Mechanism and evolution of hypoxia-tolerance in humans.

To physiologists, the term 'adaptation' usually refers to any trait that is considered advantageous; evolutionary biologists require a more rigorous definition (restricting it to traits arising and maintained under selection). By their definition, many physiological traits may merely reflect inheritance passed on through lineage. In considering the evolution of tolerance to reduced oxygen availability, we examined the issue (of true adaptations versus simple inheritance) in pinnipeds (the two dominant groups, phocids and otariids, with varying diving capacities) and in human lineages exposed for varying generational periods to hypobaric hypoxia. Basic principles of the evolution of complex physiological systems first emerged from an analysis of the diving response. We then analyzed human responses to hypobaric hypoxia in three different lineages: lowlanders, Andean natives (Quechuas) and Himalayan natives (Sherpas). As in the pinniped example, we found 'conservative' and 'adaptable' physiological characters involved in human responses to hypoxia. Conservative characters are clearly dominant and are too numerous to outline in detail; three examples are haemoglobin oxygen-affinities, the organization of muscle into different fibre types and the brain's almost exclusive preference for glucose as a fuel. Most notably, we also found evidence for 'adaptable' characters at all levels of organization examined. At the whole-body level in Quechuas and Sherpas, we found (i) that maximum aerobic and anaerobic exercise capacities were down-regulated, (ii) that the acute effect of hypoxia (making up the energy deficit due to oxygen lack; i.e. the Pasteur effect) expected from lowlanders was blunted, and (iii) that acclimation effects were also attenuated. The biochemical behaviour of skeletal muscles was consistent with lowered reliance on glycolytic contributions to energy supply, thus improving the yield of ATP per mole of carbon fuel utilized. Heart adaptations also seemed to rely upon stoichiometric efficiency adjustments, improving the yield of ATP per mole of oxygen consumed (by using glucose in preference to fatty acids). Most of the biochemical and physiological adaptations we noted (both as acute and as acclimation responses) were similar in Sherpas and Quechuas. These two lineages have not shared a common ancestor for approximately one-third of the history of our species, so it is possible that their similar physiological traits arose independently as hypoxia defence adaptations in two different times and places in our history. As in the evolution of exquisite capacities for management of oxygen down to vanishingly low levels in diving animals, the evolution of human hypoxia-tolerance can be described in terms of how two (conservative versus adaptable) categories of physiological characters are assembled in different human lineages and how the assembly changes through generational time. More recent evidence indicating that our species evolved under 'colder, drier and higher' conditions suggests that these adaptations may represent the 'ancestral' physiological condition for humans.

Adaptation, Physiological↗

PubMed2007

[Directed evolution of antibody molecules in phage-displayed combinatorial libraries].

Advances in methods for conformational prediction, structural analysis and site-directed mutagenesis of proteins and peptides have contributed to the understanding of their structure and function. However, with the exception of a few successes, the generation of practical functional molecules solely by rational design remains a difficult challenge. The aim of our study is to investigate molecular design relying on evolutionary processes, called as "directed evolution", to generate a novel class of biofunctional molecules. This evolutionary approach consists of three steps; 1) constructions of protein/peptide libraries based on structural information, 2) expressions of the libraries on phage particles, and 3) selections with investigator-imposed selective pressures. In this work, we study on directed evolution with antibody libraries. We have succeeded in generating highly active catalytic antibodies in phage-displayed antibody (Fab) libraries. To evolve catalytic antibodies toward higher catalytic activity, we have mimicked an enzyme-evolutional process, in which an enzyme has evolved their ability to use binding energies for catalysis by increasing the affinity for the transition state of a reaction and decreasing the affinity for the ground state. Thus, phage-displayed libraries derived from an original catalytic antibody were selected against a newly-devised TSA, which was programmed to optimize the differential affinity for the transition state relative to the ground state, to provide variants with improved reaction rates (k(cat)). The in vitro evolution has great potential for generating novel catalysts as well as for providing opportunities to examine the evolutionary dynamics of enzymes.

Antibodies↗

PubMed2006

Modular evolution and increase of functional complexity in replicating RNA molecules.

At early stages of biochemical evolution, the complexity of replicating molecules was limited by unavoidably high mutation rates. In an RNA world, prior to the appearance of cellular life, an increase in molecular length, and thus in functional complexity, could have been mediated by modular evolution. We describe here a scenario in which short, replicating RNA sequences are selected to perform a simple function. Molecular function is represented through the secondary structure corresponding to each sequence, and a given target secondary structure yields the optimal function in the environment where the population evolves. The combination of independently evolved populations may have facilitated the emergence of larger molecules able to perform more complex functions (including RNA replication) that could arise as a combination of simpler ones. We quantitatively show that modular evolution has relevant advantages with respect to the direct evolution of large functional molecules, among them the allowance of higher mutation rates, the shortening of evolutionary times, and the very possibility of finding complex structures that could not be otherwise directly selected.

Computational Biology↗

PubMed1991

The neutral theory of molecular evolution: a review of recent evidence.

In sharp contrast to the Darwinian theory of evolution by natural selection, the neutral theory claims that the overwhelming majority of evolutionary changes at the molecular level are caused by random fixation (due to random sampling drift in finite populations) of selectively neutral (i.e., selectively equivalent) mutants under continued inputs of mutations. The theory also asserts that most of the genetic variability within species at the molecular level (such as protein and DNA polymorphism) are selectively neutral or very nearly neutral and that they are maintained in the species by the balance between mutational input and random extinction. The neutral theory is based on simple assumptions, enabling us to develop mathematical theories based on population genetics to treat molecular evolution and variation in quantitative terms. The theory can be tested against actual observations. Neo-Darwinians continue to criticize the neutral theory, but evidence for it has accumulated over the last two decades. The recent outpouring of DNA sequence data has greatly strengthened the theory. In this paper, I review some recent observations that strongly support the neutral theory. They include such topics as pseudoglobin genes of the mouse, alpha A-crystallin genes of the blind mole rat, genes of influenza A virus and nuclear vs. mitochondrial genes of fruit flies. I also discuss such topics as the evolution of deviant coding systems in Mycoplasma, the origin of life and the unified understanding of molecular and phenotypic evolution. I conclude that since the origin of life on Earth, neutral evolutionary changes have predominated over Darwinian evolutionary changes, at least in number.

Animals↗

PubMed1993

Evolution of repeated sequences in non-coding regions of the genome.

Repeated sequences are found ubiquitously in the eukaryotic genome. Population genetic studies on the evolution of such repeated sequences are reviewed while paying special attention to those sequences found in the non-coding regions of the genome. Specifically, the evolution of dispersed repeated sequences by the transposition as well as the evolution of short tandemly repeated sequences due to either replication slippage or unequal sister chromatid exchange are considered. The approach of combining both model and data analyses which has been successfully employed in the development of the neutral theory is also considered to be useful in better understanding the evolution and biological meaning of these sequences.

Animals↗

PubMed2006

The genetic basis of thermal reaction norm evolution in lab and natural phage populations.

Two major goals of laboratory evolution experiments are to integrate from genotype to phenotype to fitness, and to understand the genetic basis of adaptation in natural populations. Here we demonstrate that both goals are possible by re-examining the outcome of a previous laboratory evolution experiment in which the bacteriophage G4 was adapted to high temperatures. We quantified the evolutionary changes in the thermal reaction norms--the curves that describe the effect of temperature on the growth rate of the phages--and decomposed the changes into modes of biological interest. Our analysis indicated that changes in optimal temperature accounted for almost half of the evolutionary changes in thermal reaction norm shape, and made the largest contribution toward adaptation at high temperatures. Genome sequencing allowed us to associate reaction norm shape changes with particular nucleotide mutations, and several of the identified mutations were found to be polymorphic in natural populations. Growth rate measures of natural phage that differed at a site that contributed substantially to adaptation in the lab indicated that this mutation also underlies thermal reaction norm shape variation in nature. In combination, our results suggest that laboratory evolution experiments may successfully predict the genetic bases of evolutionary responses to temperature in nature. The implications of this work for viral evolution arise from the fact that shifts in the thermal optimum are characterized by tradeoffs in performance between high and low temperatures. Optimum shifts, if characteristic of viral adaptation to novel temperatures, would ensure the success of vaccine development strategies that adapt viruses to low temperatures in an attempt to reduce virulence at higher (body) temperatures.

Base Sequence↗

PubMed2006

Detecting non-Brownian trait evolution in adaptive radiations.

Many phylogenetic comparative methods that are currently widely used in the scientific literature assume a Brownian motion model for trait evolution, but the suitability of that model is rarely tested, and a number of important factors might affect whether this model is appropriate or not. For instance, we might expect evolutionary change in adaptive radiations to be driven by the availability of ecological niches. Such evolution has been shown to produce patterns of change that are different from those modelled by the Brownian process. We applied two tests for the assumption of Brownian motion that generally have high power to reject data generated under non-Brownian niche-filling models for the evolution of traits in adaptive radiations. As a case study, we used these tests to explore the evolution of feeding adaptations in two radiations of warblers. In one case, the patterns revealed do not accord with Brownian motion but show characteristics expected under certain niche-filling models.

Adaptation, Biological↗