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Gene duplication as a mechanism of genomic adaptation to a changing environment

Fyodor A. Kondrashov

Proceedings of the Royal Society B: Biological Sciences · 2012 · Review

doi:10.1098/rspb.2012.1108

Abstract

A subject of extensive study in evolutionary theory has been the issue of how neutral, redundant copies can be maintained in the genome for long periods of time. Concurrently, examples of adaptive gene duplications to various environmental conditions in different species have been described. At this point, it is too early to tell whether or not a substantial fraction of gene copies have initially achieved fixation by positive selection for increased dosage. Nevertheless, enough examples have accumulated in the literature that such a possibility should be considered. Here, I review the recent examples of adaptive gene duplications and make an attempt to draw generalizations on what types of genes may be particularly prone to be selected for under certain environmental conditions. The identification of copy-number variation in ecological field studies of species adapting to stressful or novel environmental conditions may improve our understanding of gene duplications as a mechanism of adaptation and its relevance to the long-term persistence of gene duplications.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 16, 2026. Paragraph numbers are ours, so an answer can point at one.

Motivation

Few dispute that gene duplication is the main source of functional diversity on the genotype level. The wealth of sequence data to this effect has been preceded by theoretical considerations that it is far easier to create new functions from pre-existing ones rather than from scratch. At the heart of the interest towards gene duplications is the principle that after a duplication ‘each copy can evolve independently and diversify their effects’ [, p. 64] leading to functional novelty. As any mutation, a duplication event by itself may also have consequences on organism's fitness. However, two factors overshadowed the study of the short-term immediate fitness effects of gene duplication. First, the contrast in the difficulties in studying copy-number variation (CNV) that persist to this day, and the abundance of long-term evolutionary data on paralogous sequence divergence shifted the attention to where the data were. Second, and perhaps crucially, the conceptual appeal of gene duplications leading to novel functions was strong enough to overshadow that of the short-term implications of duplications.

The trend of focusing on the long-term implication to the detriment of the study of short-term effects was initiated by Ohno when he proposed that extra gene copies are redundant. His reasoning was that since one copy already performs the necessary function extra copies are redundant and free from selection, as they do not add anything to the organism's capacity in performing this function. As it became clearer that gene copies of various degree of divergence are present in genomes, the main question in the field became how can completely redundant gene copies be maintained in the genome long enough to evolve into a new function without being eliminated by mutation. Thus, the theoretical community made extensive use of the redundancy hypothesis with a string of papers looking at this question in some detail with many models not formally taking account the process of fixation of a segregating gene duplication.

At the same time, data from the microbiological community were being published suggesting adaptive impacts of gene duplications under certain environmental conditions (see for review); however, these data remain largely anecdotal and have not led to a genome-wide survey of selection on gene copy number. The diversification of the community into those that study the short-term versus the long-term effects of gene duplication may have had a linguistic component as some researchers tended to discuss ‘gene duplication’, while others studied ‘gene amplification’ with the relevant papers rarely being cross-cited. However, the fascination with the long-term consequences and the simplicity of the complete redundancy hypothesis, which essentially created the neutral theory of gene duplications, resonated in the community at the time when the neutral theory was popular and few authors took into account the adaptive point of view.

Although it is clear that some gene duplications have been fixed in the course of evolution by positive selection, whether or not it plays a significant role in the fixation of an appreciable fraction of gene duplications has yet to be comprehensively addressed at a genome-wide scale. The purpose of this review is to highlight recently described examples of adaptive short-term effects of gene duplication. Given recent reviews on whole genome duplication, negative impact of gene duplications and various theories and models on gene duplications, I will avoid these issues here.

Duplication and dosage

The main issue behind whether or not positive selection for an environmental adaptation can be the driving force behind the fixation of gene duplications is whether or not gene duplications are truly redundant. Under the verbal model commonly attributed to Ohno, the variable that affects fitness is an abstract, qualitative function, such that a gene either performs a function or not. By contrast, the adaptive hypothesis holds that function is a quantitative measure of gene action that can be influenced by the amount of gene product in the cell, which in turn can be influenced by the gene copy number. However, even if the dosage of the product in the cell influences function, it is possible that a gene duplication is still quantitatively redundant if the product dosage is tightly regulated by negative feedback loops that keep the product dosage constant against gene copy number.

In the last few years, data accumulated demonstrating that while a gene duplication may not necessarily double gene dosage, it still generally leads to its increase. It thus seems that one of the ways in which a new gene copy number may affect function is through a quantitative gene dosage effect. The complete redundancy model may still stand based on the possibility that even if dosage is increased the increase does not have an effect on fitness. The evidence against this notion is patchy and not genome-wide. However, several authors have made the claim that many CNVs are selected against in the genome owing to an increase in gene dosage, including cases of CNVs contributing to disease and, therefore, will not be discussed here. At the very least, the data seem to show that situations when a gene duplication affects gene dosage and this, in turn, affects fitness are common. Other mechanisms that can lead to an adaptive response of a gene duplication have been described; however, the dosage response is conceptually the simplest and for the purposes of this review it is assumed that the fitness effect of a gene duplication, when present, lies primarily in that the increased copy number causes an increase in protein dosage.

Adaptive gene duplications

Three genomic approaches may detect the action of selection on a specific gene duplication. Unfortunately, all three of these approaches have their limitations. First, one can study whether or not recent copies with equal function are maintained by selection by measuring the ratio of non-synonymous to synonymous evolution (dN/dS) between diverging sequences. If both are maintained by negative selection, then their initial emergence may have occurred through the action of positive selection. The logic is based on the argument that if a substitution A > G is deleterious then reverse G > A substitution is beneficial. Similarly, if in a gene copy dN/dS < 1, indicating that it is currently under negative selection and that its deletion is likely to be deleterious, then contingent on the frequency of gain-of-function mutations and lack of a new function its emergence may have been beneficial. However, when comparing very closely related gene copies with low sequence divergence, which is necessary to reduce the likelihood of this copy already performing a new function, it is not possible to measure a statistically significant departure from neutrality based on just a few substitutions, rendering the dN/dS measure relatively useless. Additionally, when comparing the dN/dS between diverged gene copies, it is possible that a measurement of dN/dS < 1 reflects selection maintaining a novel function that emerged in the process of the duplication divergence rather than selection maintaining two copies with identical function. Thus, while many studies of dN/dS between gene copies purport to reveal the action of one mechanism or other in the early evolution of gene duplications such data do not necessarily provide convincing evidence for or against the action of positive selection in the fixation of such copies. Of course, it may be possible to test whether or not very recent gene copies are under selection by looking at the ratio of non-synonymous-to-synonymous polymorphisms in the same manner as dN/dS looks at the ratio of substitutions. However, in order to apply this approach, it is necessary to sequence the gene copies independently of each other, which is not possible with currently available sequencing technologies.

The second approach is to measure the levels of variability around the emerging gene copy and search for traces of hitchhiking effects. Only one study in Arabidopsis thaliana successfully applied this approach and found evidence of hitchhiking around recent gene copies. However, this remains to my knowledge the only study of this type, possibly owing to the difficulties associated with assembling very recent gene duplications in whole genomes, which is generally necessary for such a study.

Finally, given enough data on fixed gene duplications and segregating CNVs, it may be possible to perform a McDonald–Kreitman test to try to quantify the fraction of gene copies fixed by positive selection. This was crudely done several years ago, and the results remain unconvincing owing to the complications in finding a genome-wide set of accurately annotated polymorphic gene duplications to apply the test. It is likely that different genes duplicate at different rates due to difference in length and the influence of short repeats that may substantially increase the rate of duplication of a DNA segment located between them. This issue is coupled to the relative difficulty in identifying polymorphic versus fixed gene copies in genomes. Thus, picking the right set of duplicated and polymorphic gene copies for a non-biased analysis may not be feasible at this point.

In sum, because it does not yet appear possible to systematically test the possibility of positive selection driving the fixation of gene duplications, we may study only specific cases and attempt to make generalizations based on them.

Transport of nutrients

Nutrient limitation has been observed in many species under different conditions and has been reviewed previously. A clear example of a gene duplication conferring an adaptive response to nutrient limitation is that of the yeast hexose transporter. Under growth conditions with low glucose, the appearance of a new hybrid copy from two closely related paralogues, HXT6 and HXT7, increases the level of expression of the hexose transporter and, crucially, the rate of glucose transport into the cell. Furthermore, the authors have shown in competition experiments that the strain with the gene duplication outcompetes the parental strain. The reason why this case is particularly exemplary is because the duplicated HXT6 and HXT7 genes are recent gene duplications themselves, with several more distantly related paralogoues in the genome. It is therefore just a simple step from the experiments of Brown et al. to the hypothesis that the paralogues HXT6 and HXT7 have appeared as a result of an adaptive duplication owing to selection favouring extra dosage of the transporters of glucose under various stressful or low-glucose environmental conditions. Extensive experiments carried out by Gresham et al. also show that many strains evolve amplifications either of the HXT6 or the sHXT7 gene in glucose-limited populations, although some strains adapted to starvation by different mechanisms.

Protection from heat

Adaptation to heat stress has been shown to occur through gene duplication of several stress-related genes in Escherichia coli. Some but not all of the genes contained in the duplicated regions showed increased levels of expression and the duplication events coincided with substantial increases in fitness, although not explaining all of it. Furthermore, the duplication of evgA, a master transcriptional regulator that is a part of the signal transduction system and upregulates 37 genes, allowed E. coli to withstand temperatures of over 50°C. The molecular mechanisms behind such robustness to heat remain unclear. Similar observations have been made in yeast and Arabidopsis, such that strains subjected to selection in high temperatures showed an increase propensity for chromosomal segmental duplications.

Protection from cold

A study of the genome-wide expression levels and the corresponding copy numbers provides convincing evidence for cold adaptations in Antarctic cod. In addition to the expansion of the antifreeze glycoprotein (AFGP) gene family in this species a comparison of the levels of expression between the Antarctic cod and its warm water dwelling relatives revealed 177 genes with substantial overexpression in the Antarctic cod. Through DNA hybridization, it was shown that 118 genes, many of which were from the same set with upregulated expression, have been duplicated in the Antarctic cod, some of them hundreds of times. Duplications were 10 times more common in Antarctic cod suggesting that upregulation through gene duplication of many different functions, including the well-characterized AFGP genes and FBP32II, an F-type lectin that is considered to be a close relative of the fish type II antifreeze proteins, played a role in cold adaptation of this species.

Dosage balance and restoration of fitness

Genes rarely act in isolation and it is thought that an optimal dosage of interacting proteins must be maintained for maximal fitness. This logic has been applied to explain why interacting proteins are more likely to be retained together after the whole genome duplication in yeast, however, it is also possible that a gene duplication may be favourable because it restores the correct dosage balance in a dosage sensitive system. Two such examples are found in the literature. In yeast, there are two pairs of closely related paralagous histone H2A and H2B proteins, coded by the HTA1–HTB1 and HTA2–HTB2 tandem genes pairs, respectively. When the dosage of the H2A and H2B drops owing to the deletion of the HTA1–HTB1 locus, one of the compensatory mechanisms restoring normal dosage and phenotype is a duplication of the paralagous HTA2–HTB2 locus.

Another interesting case was described by Pränting & Andersson. In Salmonella typhimurium, a mutation in a haem-biosynthesis enzyme (hemC) increases resistance of the bacterium to protamine, however, this resistance comes at a cost of the reduction of growth. In the course of a laboratory evolution experiment, the first step of a series of events after the fixation of the resistance mutation was the amplification of the mutant hemC gene that restored some of the fitness. Once the gene accumulated other compensatory point mutations that created a hemC gene that conferred resistance to protamine, but without the reduction in the rate of growth, the gene copy number was restored to normal. A similar adaptive response to the reduced fitness of a mutation leading to antibiotic resistance and a subsequent transitory compensatory increase in gene copy number of the mutated gene was found in Salmonella enterica.

Protection from salt

Adaptation to stress by high salt content may also occur through gene duplication. In one selection experiment, an increase in expression of several stress-response genes was observed, however, this increase does not appear to have anything to do with individual gene duplications as such were generally not observed in the course of the experiment. However, a consistent polyploidy of the yeast strains was observed that may play a role in the adaptation. Similarly, polyploidy has been linked to resistance to high salt concentrations in citrus and sorghum suggesting that polyploidy may be a general physiological adaptive response to osmotic stress.

Heavy metals

Duplication-induced metal resistance in different species seems to be related mainly to the export of the cations outside the cell. Among recent publications, a study showed that Ralstonia pickettii adapted to high copper concentrations in copper-contaminated lake sediment tends to accumulate the copper in the outer membrane, and the genome revealed the duplication of a region with several metal resistance and transporter genes. A detailed analysis of genome evolution of Cupriavidus metallidurans, a species particularly renowned for its tolerance of heavy metals, revealed two primary mechanisms, the increase in copy number of genes responsible for metal efflux, through HGT and duplication, and a general decrease in metal uptake. A particular strain of the fungal pathogen Cryptococcus neoformans, var. grubii subclade VNI A5 MLST, was found to contain a tandem array of several copies of the arsenite efflux transporter that confers copy-number-correlated levels of arsenite resistance.

Antibiotics and drugs

Many bacteria amplify genes as an adaptive response to antibiotic treatment. Similarly, it is commonly acknowledged that gene amplifications are known to occur in cancer tumours in response to various drug treatments (see Kondrashov & Kondrashov for review). However, the amplification of genes in response to various drug treatments is not limited to somatic cells and microbes. In the last several years, abundant data have been collected on the amplification of genes in response to various treatments of Leishmania and malaria. The Plasmodium falciparum multidrug resistance gene (pfmdr1) is a target of adaptive evolution in nature in response to the widespread use of chloroquine and other anti-malarial drugs. The pfmdr1 protein is an ABC transporter involved in the transport of chloroquine outside of the cell, however, it is more directly involved in the adaptation of the malaria parasite to mefloquine, a different anti-malarial drug. Interestingly, pfmdr1 is a homologue of the human multiple drug resistance (mdr) protein that in tumours has a crucial role of expulsion of different drugs from the cell. The pfmdr1 gene is amplified in P. falciparum in response to anti-malarial drug treatment, which can confer resistance to mefloquine and other anti-malarial drugs. It is now understood that pfmdr1 gene duplication occurred independently in nature multiple times, and malaria with increased resistance to different drugs is found throughout the world from Africa to Asia and South America. Finally, at least one amplification event of the pfmdr1 gene shows evidence of having occurred through the action of positive selection and adaptive amplification in P. falciparum has been shown in at least one other gene, GTP-cyclohydrolase I (gch1), which is involved in the synthesis of substrates upstream of other enzymes that are commonly targeted by antifolate drugs.

Gene amplification as a mechanism of adaptation to drugs is also common in Leishmania. The amplifications of the genes generally occur as extra-chromosomal circular DNA units, possibly due to the relatively minor role of transcription initiation in this organism. This may be the reason why gene amplification and the subsequent increase in gene dosage seem to be a common basis for Leishmania being resistant to different drugs. A genome-wide assay of E. coli strain in 237 toxic environments, mostly antibiotics, found 115 genes an artificial amplification of which leads to the increased fitness in the toxic environments. As with the case of metal toxicity, the function that most widely corresponded to an increase in fitness under the toxic condition was that of efflux pumps and transporters closely followed by genes with regulatory functions and many of the identified genes have not been previously implicated in toxic response. Furthermore, the amplification of several genes conferred resistance in more than one toxic environment suggesting a wider role of promiscuous functions in the evolution of resistance.

Pesticides and complex organic compounds

The application of pesticides and herbicides promotes the adaptive duplication of enzymes that digest the chemical ( and see for review). A well-studied example is that of the mosquito Culex pipiens that was subject to pesticide treatment on the southern coast of France. Adaptation to pesticide treatment evolved by the duplication of two non-specific esterases (Est-2 and Est-3), and Ace.1, a locus encoding acetylcholinesterase that is the main target of the applied organo-phosphate insecticides. However, the duplication of Ace.1 comes at a substantial fitness cost, which has led to intricate evolutionary dynamics in the evolution of this locus with subsequent duplications being maintained in heterozygous states across the population owing to a low fitness of the duplications in homozygous state. Furthermore, similar to the strong selection pressure of the anti-malarial drugs leading to independent multiple duplications of the pfmdr1 gene, the Ace.1 resistance duplication also appeared multiple times independently around the world. The combination of independent origin and the persistence of the duplication in heterozygous form despite the low fitness of homozygous states indicate positive selection for the original emergence of the heterozygous duplication.

Adaptation to domestication

Different cow breeds have been analysed for differences in CNVs with different functional families featuring prominently in the differences. First, CNVs of immune-related genes coding for UL16-binding proteins have been described in different breeds of cattle and fixed copies of these genes have been shown to be duplicated in the recent ancestor of the Bos lineage. Furthermore, recently duplicated genes have been associated with recent domestication-related phenotypes such as milk proteins and proteins related to ruminant digestion. A recent genome-wide study of three cattle breeds identified approximately 400 genes located in CNVs, many of which were related to different environmental interaction and domestication related functions, including parasite and pathogen resistance, lipid transport and metabolism. In a few cases, the types of gene function could be linked to breed-specific phenotypes, suggesting that several aspects of cattle health and productivity have been selected through CNV in the course of cattle domestication.

Adaptive duplications in humans

In our own species, several examples have been described of a polymorphic duplication conferring either a distinct phenotype or a fitness advantage. Thus, individuals with more copies of the CCL3L1 gene, a ligand for the HIV-suppressive CC chemokine receptor, have lower susceptibility to HIV infection and slower progression to AIDS after infection. A widely reviewed example is that of the salivary amylase gene (AMY1) that plays a role in the initiation of starch digestion. Individuals from populations with higher starch content in their traditional diets have a higher copy number of this protein providing an apparent fitness benefit. The high prevalence of CNV in the human genome coupled with data that many of them may be adaptive, suggest that more examples of adaptive gene duplication in the human population are yet to be described.

Generalizations

Adaptive duplications in different species continue to be described in the literature (see table 1 for additional examples) implying that gene duplication as a form of adaptation to various environmental conditions is not a rare mechanism, although by far not an exclusive one. Perhaps several generalizations can be made regarding when an adaptive duplication may be expected to play a role in various adaptations in nature. First, in instances when the protein products of the genes physically interact with molecules associated with a variable environment such as toxins or nutrients. Second, when the proteins coded by the duplicated genes function in the same pathway as those that physically interact with such molecules. Finally, adaptive duplication seems to involve those genes which product needs to be produced rapidly or constantly at a high level, such as antifreeze or storage proteins.

The main logic for hypothesizing that fixed gene duplications played an adaptive role in dosage response to stressful environment has been the functions of gene duplications with characterized adaptive role and the functions of fixed gene copies that are observed in the genome. However, it may be instructive to reverse the logic and predict the types of genes that may confer an adaptation in some environmental conditions based on the functional repertoire of the gene duplications observed in the genome.

One of the main duplicated gene families are the olfactory receptor proteins so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions. The match in the sensitivity range of duplicated opsin genes and coloration suggests that the duplication of an opsin gene may cause an adaptive increase in sensitivity to light of a certain wavelength. Duplications of genes involved in pathogen resistance and pathogenicity suggest that gene duplications may have a role in rapid coevolution between host and pathogen or symbiont. Recent gene duplications in drought-resistant plants suggest that genes involved in osmotic stress response are also good candidates. Duplication of the globin genes may be adaptive in low-oxygen environments, such as high altitude, by optimizing oxygen transport. Common duplications of different defence toxins and venoms suggest that toxin dosage and their effectiveness may be regulated through gene duplication. Similarly, the duplication of proteins involved in the degradation of toxins, for example enzymes that neutralize pyrrolizidine alkaloids, may confer a fitness advantage to a herbivore feeding on a plant with high concentration of specific toxins. The duplication of developmentally related genes may confer an adaptive advantage in the anatomical modification of the body plan for a new environment. The production of carotenoids or light emission by luciferase may be dosage-mediated by gene duplication leading to extra pigment or higher intensity of light. The duplication of proteases expressed in the female reproductive tract of Drosophila mojavensis and sperm-related proteins in Caenorhabditis elegans suggests that dosage increase through gene duplication may be adaptive as a strategy in sexual conflict.

Discussion

The development of the theory of gene duplications reflects that of the neutral theory of molecular evolution. The strong claim of neutrality of gene duplications made by Ohno reflected a point of view that all gene duplications are neutral. Most theoretical models that followed maintained that the redundancy of the gene duplication leads to its neutrality. In the last few years, it became evident that many gene duplications are deleterious from the moment of their origin. However, this can be easily accommodated in the redundancy-based theories on long-term evolution of gene duplication in the form of a weak claim of neutrality: those gene duplications that are fixed are neutral. Because no quantitative genome-wide estimates of the fraction of gene duplications that are fixed by positive selection have been made, population genetic theories explaining the evolution of gene duplication have not incorporated selection on gene copy number in the models.

At the present moment, the literature reflects a point of view that gene duplications are more neutral than amino acid substitutions. A large fraction of amino acid substitutions is thought to be fixed by positive selection, yet most authors continue to explain the origin and maintenance of gene duplications by referring to theories of their maintenance that assume complete redundancy and a neutral path to fixation. However, presumably a gene duplication is mutation of stronger impact than a point mutation and, therefore, it should on average have a more profound impact on fitness than a substitution. This somewhat paradoxical situation is reflected in the literature on CNVs where authors avoid reference to the existing theories on gene duplication.

Owing to the fascination with the idea of complete genetic redundancy, classical population genetic and evolutionary models of gene duplications generally failed to be useful in the description of CNV in natural population (but see). Perhaps the same fate of irrelevance awaits the theoretical field once ecological genomics starts addressing the question of adaptation to stressful environmental conditions on a genome-wide scale in multiple non-model organisms. To model such adaptation, the necessary theoretical models may be more complicated than those simply incorporating a quantitative measure of genetic redundancy as they may also have to be time-dependent; in several cases, it appears that a gene duplication that is adaptive under a stressful condition comes at a fitness cost in a benign environment.

The cost and utility of sequencing technology makes it possible to obtain a genome sequence of reasonable quality for all but the most complicated genomes. The application of such technology to natural populations is bound to reveal new mechanisms of ecological adaptation. Given the abundance of examples of adaptive gene duplications that emerge in the course of adaptation to stressful environments, researchers studying the adaptation of species to novel or stressful environments would be well advised to consider taking a closer look at recent gene duplications and copy-number polymorphisms. Meanwhile, the relative role of positive selection versus drift in fixation of gene duplications remains an open question.

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    Innan H. Kondrashov F. 2010 The evolution of gene duplications: classifying and distinguishing between models. Nat. Rev. Genet. 11, 97–108 (doi:10.1038/nrg2689)

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    Schuster-Böckler B. Conrad D. Bateman A. 2010 Dosage sensitivity shapes the evolution of copy-number varied regions. PLoS ONE 5, e9474 (doi:10.1371/journal.pone.0009474)

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    Stranger B. E. 2007 Relative impact of nucleotide and copy number variation on gene expression phenotypes. Science 315, 848–853 (doi:10.1126/science.1136678)

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    Zhou J. Lemos B. Dopman E. B. Hartl D. L. 2011 Copy-number variation: the balance between gene dosage and expression in Drosophila melanogaster. Genome Biol. Evol. 3, 1014–1024 (doi:10.1093/gbe/evr023)

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    Kondrashov F. A. Kondrashov A. S. 2006 Role of selection in fixation of gene duplications. J. Theor. Biol. 239, 141–151 (doi:10.1016/j.jtbi.2005.08.033)

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    Lupski J. R. 2007 An evolution revolution provides further revelation. Bioessays 29, 1182–1184 (doi:10.1002/bies.20686)

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    Moore R. C. Purugganan M. D. 2003 The early stages of duplicate gene evolution. Proc. Natl Acad. Sci. USA 100, 15 682–15 687 (doi:10.1073/pnas.2535513100)

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  39. 39.

    McDonald J. H. Kreitman M. 1991 Adaptive protein evolution at the Adh locus in Drosophila. Nature 351, 652–654 (doi:10.1038/351652a0)

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    Shaw C. J. Lupski J. R. 2004 Implications of human genome architecture for rearrangement-based disorders: the genomic basis of disease. Hum. Mol. Genet. 13, R57–R64 (doi:10.1093/hmg/ddh073)

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  41. 41.

    Brown C. J. Todd K. M. Rosenzweig R. F. 1998 Multiple duplications of yeast hexose transport genes in response to selection in a glucose-limited environment. Mol. Biol. Evol. 15, 931–942 (doi:10.1093/oxfordjournals.molbev.a026009)

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  42. 42.

    Lin Z. Li W. H. 2011 Expansion of hexose transporter genes was associated with the evolution of aerobic fermentation in yeasts. Mol. Biol. Evol. 28, 131–142 (doi:10.1093/molbev/msq184)

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  43. 43.
    The Repertoire and Dynamics of Evolutionary Adaptations to Controlled Nutrient-Limited Environments in Yeast · 2008
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  44. 44.
    Genetic architecture of thermal adaptation in Escherichia coli · 2001
    Not checked
  45. 45.

    Christ D. Chin J. W. 2008 Engineering Escherichia coli heat-resistance by synthetic gene amplification. Protein Eng. Des. Sel. 21, 121–125 (doi:10.1093/protein/gzm085)

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  46. 46.

    James T. C. Usher J. Campbell S. Bond U. 2008 Lager yeasts possess dynamic genomes that undergo rearrangements and gene amplification in response to stress. Curr. Genet. 53, 139–152 (doi:10.1007/s00294-007-0172-8)

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  47. 47.

    DeBolt S. 2010 Copy number variation shapes genome diversity in Arabidopsis over immediate family generational scales. Genome Biol. Evol. 2, 441–453 (doi:10.1093/gbe/evq033)

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  48. 48.

    Chen L. DeVries A. L. Cheng C. H. 1997 Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish. Proc. Natl Acad. Sci. USA 94, 3811–3816 (doi:10.1073/pnas.94.8.3811)

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  49. 49.

    Chen Z. 2008 Transcriptomic and genomic evolution under constant cold in Antarctic notothenioid fish. Proc. Natl Acad. Sci. USA 105, 12 944–12 949 (doi:10.1073/pnas.0802432105)

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  50. 50.

    Papp B. Pál C. Hurst L. D. 2003 Dosage sensitivity and the evolution of gene families in yeast. Nature 424, 194–197 (doi:10.1038/nature01771)

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  51. 51.

    Libuda D. E. Winston F. 2006 Amplification of histone genes by circular chromosome formation in Saccharomyces cerevisiae. Nature 443, 1003–1007 (doi:10.1038/nature05205)

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  52. 52.

    Pränting M. Andersson D. I. 2011 Escape from growth restriction in small colony variants of Salmonella typhimurium by gene amplification and mutation. Mol. Microbiol. 79, 305–315 (doi:10.1111/j.1365-2958.2010.07458.x)

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  53. 53.

    Paulander W. Andersson D. I. Maisnier-Patin S. 2010 Amplification of the gene for isoleucyl-tRNA synthetase facilitates adaptation to the fitness cost of mupirocin resistance in Salmonella enterica. Genetics 185, 305–312 (doi:10.1534/genetics.109.113514)

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  54. 54.

    Dhar R. Sägesser R. Weikert C. Yuan J. Wagner A. 2011 Adaptation of Saccharomyces cerevisiae to saline stress through laboratory evolution. J. Evol. Biol. 24, 1135–1153 (doi:10.1111/j.1420-9101.2011.02249.x)

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  55. 55.
    Genomic Convergence toward Diploidy in Saccharomyces cerevisiae · 2006
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  56. 56.

    Saleh B. Allario T. Dambier D. Ollitrault P. Morillon R. 2008 Tetraploid citrus rootstocks are more tolerant to salt stress than diploid. C. R. Biol. 331, 703–710 (doi:10.1016/j.crvi.2008.06.007)

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  57. 57.

    Ceccarelli M. Santantonio E. Marmottini F. Amzallag G. N. Cionini P. G. 2006 Chromosome endoreduplication as a factor of salt adaptation in Sorghum bicolor. Protoplasma 227, 113–118 (doi:10.1007/s00709-005-0144-0)

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  58. 58.

    Yang F. Pecina D. A. Kelly S. D. Kim S. H. Kemner K. M. Long D. T. Marsh T. L. 2010 Biosequestration via cooperative binding of copper by Ralstonia pickettii. Environ. Technol. 31, 1045–1060 (doi:10.1080/09593330.2010.487290)

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  59. 59.

    von Rozycki T. Nies D. H. 2009 Cupriavidus metallidurans: evolution of a metal-resistant bacterium. Antonie Van Leeuwenhoek 96, 115–139 (doi:10.1007/s10482-008-9284-5)

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  60. 60.

    Chow E. W. Morrow C. A. Djordjevic J. T. Wood I. A. Fraser J. A. 2012 Microevolution of Cryptococcus neoformans driven by massive tandem gene amplification. Mol. Biol. Evol. 29, 1987–2000 (doi:10.1093/molbev/mss066)

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  61. 61.

    Craven S. H. Neidle E. L. 2007 Double trouble: medical implications of genetic duplication and amplification in bacteria. Future Microbiol. 2, 309–321 (doi:10.2217/17460913.2.3.309)

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  62. 62.

    Sandegren L. Andersson D. I. 2009 Bacterial gene amplification: implications for the evolution of antibiotic resistance. Nat. Rev. Microbiol. 7, 578–588 (doi:10.1038/nrmicro2174)

    Not in our library10.1038/nrmicro2174

  63. 63.

    Segovia M. 1994 Leishmania gene amplification: a mechanism of drug resistance. Ann. Trop. Med. Parasitol. 88, 123–130

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  64. 64.

    Foote S. J. Thompson J. K. Cowman A. F. Kemp D. J. 1989 Amplification of the multidrug resistance gene in some chloroquine-resistant isolates of P. falciparum. Cell 57, 921–930 (doi:10.1016/0092-8674(89)90330-9)

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  65. 65.

    Foote S. J. Kyle D. E. Martin R. K. Oduola A. M. Forsyth K. Kemp D. J. Cowman A. F. 1990 Several alleles of the multidrug-resistance gene are closely linked to chloroquine resistance in Plasmodium falciparum. Nature 345, 255–258 (doi:10.1038/345255a0)

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  66. 66.

    Duraisingh M. T. Cowman A. F. 2005 Contribution of the pfmdr1 gene to antimalarial drug-resistance. Acta Trop. 94, 181–190 (doi:10.1016/j.actatropica.2005.04.008)

    Not in our library10.1016/j.actatropica.2005.04.008

  67. 67.

    Preechapornkul P. Imwong M. Chotivanich K. Pongtavornpinyo W. Dondorp A. M. Day N. P. White N. J. Pukrittayakamee S. 2009 Plasmodium falciparum pfmdr1 amplification, mefloquine resistance, and parasite fitness. Antimicrob. Agents Chemother. 53, 1509–1515 (doi:10.1128/AAC.00241-08)

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  68. 68.

    Chavchich M. Gerena L. Peters J. Chen N. Cheng Q. Kyle D. E. 2010 Role of pfmdr1 amplification and expression in induction of resistance to artemisinin derivatives in Plasmodium falciparum. Antimicrob. Agents Chemother. 54, 2455–2464 (doi:10.1128/AAC.00947-09)

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  69. 69.

    Triglia T. Foote S. J. Kemp D. J. Cowman A. F. 1991 Amplification of the multidrug resistance gene pfmdr1 in Plasmodium falciparum has arisen as multiple independent events. Mol. Cell. Biol. 11, 5244–5250

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  70. 70.

    Gadalla N. B. 2011 Increased pfmdr1 copy number and sequence polymorphisms in Plasmodium falciparum isolates from Sudanese malaria patients treated with artemether–lumefantrine. Antimicrob. Agents Chemother. 55, 5408–5411 (doi:10.1128/AAC.05102-11)

    Not in our library10.1128/aac.05102-11

  71. 71.

    Imwong M. 2008 Gene amplification of the multidrug resistance 1 gene of Plasmodium vivax isolates from Thailand, Laos, and Myanmar. Antimicrob. Agents Chemother. 52, 2657–2659 (doi:10.1128/AAC.01459-07)

    Not in our library10.1128/aac.01459-07

  72. 72.

    Meng H. Zhang R. Yang H. Fan Q. Su X. Miao J. Cui L. Yang Z. 2010 In vitro sensitivity of Plasmodium falciparum clinical isolates from the China–Myanmar border area to quinine and association with polymorphism in the Na+/H+ exchanger. Antimicrob. Agents Chemother. 54, 4306–4313 (doi:10.1128/AAC.00321-10)

    Not in our library10.1128/aac.00321-10

  73. 73.

    Griffing S. 2010 pfmdr1 amplification and fixation of pfcrt chloroquine resistance alleles in Plasmodium falciparum in Venezuela. Antimicrob. Agents Chemother. 54, 1572–1579 (doi:10.1128/AAC.01243-09)

    Not in our library10.1128/aac.01243-09

  74. 74.

    Nair S. Nash D. Sudimack D. Jaidee A. Barends M. Uhlemann A. C. Krishna S. Nosten F. Anderson T. J. 2007 Recurrent gene amplification and soft selective sweeps during evolution of multidrug resistance in malaria parasites. Mol. Biol. Evol. 24, 562–573 (doi:10.1093/molbev/msl185)

    Not in our library10.1093/molbev/msl185

  75. 75.
    Adaptive Copy Number Evolution in Malaria Parasites · 2008
    No notice
  76. 76.
    Modulation of gene expression in drug resistant Leishmania is associated with gene amplification, gene deletion and chromosome aneuploidy · 2008
    No notice
  77. 77.

    Mary C. Faraut F. Deniau M. Dereure J. Aoun K. Ranque S. Piarroux R. 2010 Frequency of drug resistance gene amplification in clinical Leishmania strains. Int. J. Microbiol. 2010, 819060 (doi:10.1155/2010/819060)

    Not in our library10.1155/2010/819060

  78. 78.

    Soo V. W. Hanson-Manful P. Patrick W. M. 2011 Artificial gene amplification reveals an abundance of promiscuous resistance determinants in Escherichia coli. Proc. Natl Acad. Sci. USA 108, 1484–1489 (doi:10.1073/pnas.1012108108)

    Not in our library10.1073/pnas.1012108108

  79. 79.

    Taylor M. Feyereisen R. 1996 Molecular biology and evolution of resistance of toxicants. Mol. Biol. Evol. 13, 719–734 (doi:10.1093/oxfordjournals.molbev.a025633)

    Not in our library10.1093/oxfordjournals.molbev.a025633

  80. 80.

    Lenormand T. Guillemaud T. Bourguet D. Raymond M. 1998 Appearance and sweep of a gene duplication: adaptive response and potential for new functions in the mosquito Culex pipiens. Evolution 52, 1705–1712 (doi:10.2307/2411343)

    Not in our library10.2307/2411343

  81. 81.

    Labbé P. Berticat C. Berthomieu A. Unal S. Bernard C. Weill M. Lenormand T. 2007 Forty years of erratic insecticide resistance evolution in the mosquito Culex pipiens. PLoS Genet. 3, e205 (doi:10.1371/journal.pgen.0030205)

    Not in our library10.1371/journal.pgen.0030205

  82. 82.

    Labbé P. Berthomieu A. Berticat C. Alout H. Raymond M. Lenormand T. Weill M. 2007 Independent duplications of the acetylcholinesterase gene conferring insecticide resistance in the mosquito Culex pipiens. Mol. Biol. Evol. 24, 1056–1067 (doi:10.1093/molbev/msm025)

    Not in our library10.1093/molbev/msm025

  83. 83.

    Alout H. Labbé P. Pasteur N. Weill M. 2011 High incidence of ace-1 duplicated haplotypes in resistant Culex pipiens mosquitoes from Algeria. Insect Biochem. Mol. Biol. 41, 29–35 (doi:10.1016/j.ibmb.2010.09.009)

    Not in our library10.1016/j.ibmb.2010.09.009

  84. 84.

    Larson J. H. Marron B. M. Beever J. E. Roe B. A. Lewin H. A. 2006 Genomic organization and evolution of the ULBP genes in cattle. BMC Genomics 7, 227 (doi:10.1186/1471-2164-7-227)

    Not in our library10.1186/1471-2164-7-227

  85. 85.

    Bickhart D. M. 2012 Copy number variation of individual cattle genomes using next-generation sequencing. Genome Res. 22, 778–790 (doi:10.1101/gr.133967.111)

    Not in our library10.1101/gr.133967.111

  86. 86.
    Analysis of recent segmental duplications in the bovine genome · 2009
    Not checked
  87. 87.

    Gonzalez E. 2005 The influence of CCL3L1 gene-containing segmental duplications on HIV-1/AIDS susceptibility. Science 307, 1434–1440 (doi:10.1126/science.1101160)

    Not in our library10.1126/science.1101160

  88. 88.

    Perry G. H. 2007 Diet and the evolution of human amylase gene copy number variation. Nat. Genet. 39, 1256–1260 (doi:10.1038/ng2123)

    Not in our library10.1038/ng2123

  89. 89.

    Cooper G. M. Nickerson D. A. Eichler E. E. 2007 Mutational and selective effects on copy-number variants in the human genome. Nat. Genet. 39, S22–S29 (doi:10.1038/ng2054)

    Not in our library10.1038/ng2054

  90. 90.

    Emerson J. J. Cardoso-Moreira M. Borevitz J. O. Long M. 2008 Natural selection shapes genome-wide patterns of copy-number polymorphism in Drosophila melanogaster. Science 320, 1629–1631 (doi:10.1126/science.1158078)

    Not in our library10.1126/science.1158078

  91. 91.

    Gazave E. 2011 Copy number variation analysis in the great apes reveals species-specific patterns of structural variation. Genome Res. 21, 1626–1639 (doi:10.1101/gr.117242.110)

    Not in our library10.1101/gr.117242.110

  92. 92.

    Hastings P. J. Bull H. J. Klump J. R. Rosenberg S. M. 2000 Adaptive amplification: an inducible chromosomal instability mechanism. Cell 103, 723–731 (doi:10.1016/S0092-8674(00)00176-8)

    Not in our library10.1016/s0092-8674(00)00176-8

  93. 93.

    Zhong S. Khodursky A. Dykhuizen D. E. Dean A. M. 2004 Evolutionary genomics of ecological specialization. Proc. Natl Acad. Sci. USA 101, 11 719–11 724 (doi:10.1073/pnas.0404397101)

    Not in our library10.1073/pnas.0404397101

  94. 94.

    Lin D. Gibson I. B. Moore J. M. Thornton P. C. Leal S. M. Hastings P. J. 2011 Global chromosomal structural instability in a subpopulation of starving Escherichia coli cells. PLoS Genet. 7, e1002223 (doi:10.1371/journal.pgen.1002223)

    Not in our library10.1371/journal.pgen.1002223

  95. 95.

    Xu J. H. Messing J. 2009 Amplification of prolamin storage protein genes in different subfamilies of the Poaceae. Theor. Appl. Genet. 119, 1397–1412 (doi:10.1007/s00122-009-1143-x)

    Not in our library10.1007/s00122-009-1143-x

  96. 96.

    Desjardins M. Graham L. A. Davies P. L. Fletcher G. L. 2012 Antifreeze protein gene amplification facilitated niche exploitation and speciation in wolffish. FEBS J. 279, 2215–2230 (doi:10.1111/j.1742-4658.2012.08605.x)

    Not in our library10.1111/j.1742-4658.2012.08605.x

  97. 97.
    Tracking the evolution of a cold stress associated gene family in cold tolerant grasses · 2008
    Not checked
  98. 98.

    Zhou D. 2009 Duplication and adaptive evolution of the COR15 genes within the highly cold-tolerant Draba lineage (Brassicaceae). Gene 441, 36–44 (doi:10.1016/j.gene.2008.06.024)

    Not in our library10.1016/j.gene.2008.06.024

  99. 99.

    Lind P. A. Tobin C. Berg O. G. Kurland C. G. Andersson D. I. 2010 Compensatory gene amplification restores fitness after inter-species gene replacements. Mol. Microbiol. 75, 1078–1089 (doi:10.1111/j.1365-2958.2009.07030.x)

    Not in our library10.1111/j.1365-2958.2009.07030.x

  100. 100.

    Widholm J. M. Chinnala A. R. Ryu J. H. Song H. S. Eggett T. Brotherton J. E. 2001 Glyphosate selection of gene amplification in suspension cultures of 3 plant species. Physiol. Plant 112, 540–545 (doi:10.1034/j.1399-3054.2001.1120411.x)

    Not in our library10.1034/j.1399-3054.2001.1120411.x

  101. 101.

    Gaines T. A. 2010 Gene amplification confers glyphosate resistance in Amaranthus palmeri. Proc. Natl Acad. Sci. USA 107, 1029–1034 (doi:10.1073/pnas.0906649107)

    Not in our library10.1073/pnas.0906649107

  102. 102.

    Gaines T. A. Shaner D. L. Ward S. M. Leach J. E. Preston C. Westra P. 2011 Mechanism of resistance of evolved glyphosate-resistant Palmer amaranth (Amaranthus palmeri). J. Agric. Food. Chem. 59, 5886–5889 (doi:10.1021/jf104719k)

    Not in our library10.1021/jf104719k

  103. 103.

    Eanes W. F. Merritt T. J. Flowers J. M. Kumagai S. Zhu C. T. 2009 Direct evidence that genetic variation in glycerol-3-phosphate and malate dehydrogenase genes (Gpdh and Mdh1) affects adult ethanol tolerance in Drosophila melanogaster. Genetics 181, 607–614 (doi:10.1534/genetics.108.089383)

    Not in our library10.1534/genetics.108.089383

  104. 104.

    Wapinski I. Pfeffer A. Friedman N. Regev A. 2007 Natural history and evolutionary principles of gene duplication in fungi. Nature 449, 54–61 (doi:10.1038/nature06107)

    Not in our library10.1038/nature06107

  105. 105.

    Hanada K. Zou C. Lehti-Shiu M. D. Shinozaki K. Shiu S. H. 2008 Importance of lineage-specific expansion of plant tandem duplicates in the adaptive response to environmental stimuli. Plant Physiol. 148, 993–1003 (doi:10.1104/pp.108.122457)

    Not in our library10.1104/pp.108.122457

  106. 106.

    Kuo C. H. Kissinger J. C. 2008 Consistent and contrasting properties of lineage-specific genes in the apicomplexan parasites Plasmodium and Theileria. BMC Evol. Biol. 8, 108 (doi:10.1186/1471-2148-8-108)

    Not in our library10.1186/1471-2148-8-108

  107. 107.

    Hoffmann F. G. Opazo J. C. Storz J. F. 2008 Rapid rates of lineage-specific gene duplication and deletion in the alpha-globin gene family. Mol. Biol. Evol. 25, 591–602 (doi:10.1093/molbev/msn004)

    Not in our library10.1093/molbev/msn004

  108. 108.

    Cornman R. S. Willis J. H. 2008 Extensive gene amplification and concerted evolution within the CPR family of cuticular proteins in mosquitoes. Insect Biochem. Mol. Biol. 38, 661–676 (doi:10.1016/j.ibmb.2008.04.001)

    Not in our library10.1016/j.ibmb.2008.04.001

  109. 109.

    Lehti-Shiu M. D. Zou C. Hanada K. Shiu S. H. 2009 Evolutionary history and stress regulation of plant receptor-like kinase/pelle genes. Plant Physiol. 150, 12–26 (doi:10.1104/pp.108.134353)

    Not in our library10.1104/pp.108.134353

  110. 110.

    Jiang S. Y. Ma Z. Ramachandran S. 2010 Evolutionary history and stress regulation of the lectin superfamily in higher plants. BMC Evol. Biol. 10, 79 (doi:10.1186/1471-2148-10-79)

    Not in our library10.1186/1471-2148-10-79

  111. 111.

    Gong D. Wilson P. W. Bain M. M. McDade K. Kalina J. Hervé-Grépinet V. Nys Y. Dunn I. C. 2010 Gallin; an antimicrobial peptide member of a new avian defensin family, the ovodefensins, has been subject to recent gene duplication. BMC Immunol. 11, 12 (doi:10.1186/1471-2172-11-12)

    Not in our library10.1186/1471-2172-11-12

  112. 112.

    Ames R. M. Rash B. M. Hentges K. E. Robertson D. L. Delneri D. Lovell S. C. 2010 Gene duplication and environmental adaptation within yeast populations. Genome Biol. Evol. 2, 591–601 (doi:10.1093/gbe/evq043)

    Not in our library10.1093/gbe/evq043

  113. 113.

    Miller S. R. Wood A. M. Blankenship R. E. Kim M. Ferriera S. 2011 Dynamics of gene duplication in the genomes of chlorophyll d-producing cyanobacteria: implications for the ecological niche. Genome Biol. Evol. 3, 601–613 (doi:10.1093/gbe/evr060)

    Not in our library10.1093/gbe/evr060

  114. 114.

    Colbourne J. K. 2011 The ecoresponsive genome of Daphnia pulex. Science 331, 555–561 (doi:10.1126/science.1197761)

    Not in our library10.1126/science.1197761

  115. 115.

    Xu J. H. Bennetzen J. L. Messing J. 2012 Dynamic gene copy number variation in collinear regions of grass genomes. Mol. Biol. Evol. 29, 861–871 (doi:10.1093/molbev/msr261)

    Not in our library10.1093/molbev/msr261

  116. 116.

    Wong E. S. Belov K. 2012 Venom evolution through gene duplications. Gene. 496, 1–7 (doi:10.1016/j.gene.2012.01.009)

    Not in our library10.1016/j.gene.2012.01.009

  117. 117.

    Nei M. Niimura Y. Nozawa M. 2008 The evolution of animal chemosensory receptor gene repertoires: roles of chance and necessity. Nat. Rev. Genet. 9, 951–963 (doi:10.1038/nrg2480)

    Not in our library10.1038/nrg2480

  118. 118.
    Evolutionary dynamics of olfactory receptor genes in chordates: interaction between environments and genomic contents · 2009
    Not checked
  119. 119.

    Lavagnino N. Serra F. Arbiza L. Dopazo H. Hasson E. 2012 Evolutionary genomics of genes involved in olfactory behavior in the Drosophila melanogaster species group. Evol. Bioinform. Online 8, 89–104 (doi:10.4137/EBO.S8484)

    Not in our library10.4137/ebo.s8484

  120. 120.

    Sison-Mangus M. P. Bernard G. D. Lampel J. Briscoe A. D. 2006 Beauty in the eye of the beholder: the two blue opsins of lycaenid butterflies and the opsin gene-driven evolution of sexually dimorphic eyes. J. Exp. Biol. 209, 3079–3090 (doi:10.1242/jeb.02360)

    Not in our library10.1242/jeb.02360

  121. 121.

    Gojobori J. Innan H. 2009 Potential of fish opsin gene duplications to evolve new adaptive functions. Trends Genet. 25, 198–202 (doi:10.1016/j.tig.2009.03.008)

    Not in our library10.1016/j.tig.2009.03.008

  122. 122.

    Schulenburg H. Boehnisch C. 2008 Diversification and adaptive sequence evolution of Caenorhabditis lysozymes (Nematoda: Rhabditidae). BMC Evol. Biol. 8, 114 (doi:10.1186/1471-2148-8-114)

    Not in our library10.1186/1471-2148-8-114

  123. 123.

    Neiman M. Olson M. S. Tiffin P. 2009 Selective histories of poplar protease inhibitors: elevated polymorphism, purifying selection, and positive selection driving divergence of recent duplicates. New Phytol. 183, 740–750 (doi:10.1111/j.1469-8137.2009.02936.x)

    Not in our library10.1111/j.1469-8137.2009.02936.x

  124. 124.

    Powell A. J. Conant G. C. Brown D. E. Carbone I. Dean R. A. 2008 Altered patterns of gene duplication and differential gene gain and loss in fungal pathogens. BMC Genomics 9, 147 (doi:10.1186/1471-2164-9-147)

    Not in our library10.1186/1471-2164-9-147

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    Fischer I. Camus-Kulandaivelu L. Allal F. Stephan W. 2011 Adaptation to drought in two wild tomato species: the evolution of the Asr gene family. New Phytol. 190, 1032–1044 (doi:10.1111/j.1469-8137.2011.03648.x)

    Not in our library10.1111/j.1469-8137.2011.03648.x

  126. 126.

    Storz J. F. Runck A. M. Sabatino S. J. Kelly J. K. Ferrand N. Moriyama H. Weber R. E. Fago A. 2009 Evolutionary and functional insights into the mechanism underlying high-altitude adaptation of deer mouse hemoglobin. Proc. Natl Acad. Sci. USA 106, 14 450–14 455 (doi:10.1073/pnas.0905224106)

    Not in our library10.1073/pnas.0905224106

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    Duda T. F. Jr Palumbi S. R. 1999 Molecular genetics of ecological diversification: duplication and rapid evolution of toxin genes of the venomous gastropod Conus. Proc. Natl Acad. Sci. USA 96, 6820–6823 (doi:10.1073/pnas.96.12.6820)

    Not in our library10.1073/pnas.96.12.6820

  128. 128.

    Moran Y. Gurevitz M. 2006 When positive selection of neurotoxin genes is missing. The riddle of the sea anemone Nematostella vectensis. FEBS J. 273, 3886–3892 (doi:10.1111/j.1742-4658.2006.05397.x)

    Not in our library10.1111/j.1742-4658.2006.05397.x

  129. 129.
    Inventing an arsenal: adaptive evolution and neofunctionalization of snake venom phospholipase A2 genes. · 2007
    No notice
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    Murray S. A. Mihali T. K. Neilan B. A. 2011 Extraordinary conservation, gene loss, and positive selection in the evolution of an ancient neurotoxin. Mol. Biol. Evol. 28, 1173–1182 (doi:10.1093/molbev/msq295)

    Not in our library10.1093/molbev/msq295

  131. 131.

    Ma Y. He Y. Zhao R. Wu Y. Li W. Cao Z. 2012 Extreme diversity of scorpion venom peptides and proteins revealed by transcriptomic analysis: implication for proteome evolution of scorpion venom arsenal. J. Proteomics 75, 1563–1576 (doi:10.1016/j.jprot.2011.11.029)

    Not in our library10.1016/j.jprot.2011.11.029

  132. 132.

    Chang D. Duda T. F. Jr 2012 Extensive and continuous duplication facilitates rapid evolution and diversification of gene families. Mol. Biol. Evol. 29, 2019–2029 (doi:10.1093/molbev/mss068)

    Not in our library10.1093/molbev/mss068

  133. 133.

    Wang L. Beuerle T. Timbilla J. Ober D. 2012 Independent recruitment of a flavin-dependent monooxygenase for safe accumulation of sequestered pyrrolizidine alkaloids in grasshoppers and moths. PLoS ONE 7, e31796 (doi:10.1371/journal.pone.0031796)

    Not in our library10.1371/journal.pone.0031796

  134. 134.

    Shigenobu S. 2010 Comprehensive survey of developmental genes in the pea aphid, Acyrthosiphon pisum: frequent lineage-specific duplications and losses of developmental genes. Insect Mol. Biol. 19(Suppl. 2), 47–62 (doi:10.1111/j.1365-2583.2009.00944.x)

    Not in our library10.1111/j.1365-2583.2009.00944.x

  135. 135.

    Moran N. A. Jarvik T. 2010 Lateral transfer of genes from fungi underlies carotenoid production in aphids. Science 328, 624–627 (doi:10.1126/science.1187113)

    Not in our library10.1126/science.1187113

  136. 136.

    Day J. C. Goodall T. I. Bailey M. J. 2009 The evolution of the adenylate-forming protein family in beetles: multiple luciferase gene paralogues in fireflies and glow-worms. Mol. Phylogenet. Evol. 50, 93–101 (doi:10.1016/j.ympev.2008.09.026)

    Not in our library10.1016/j.ympev.2008.09.026

  137. 137.

    Kelleher E. S. Markow T. A. 2009 Duplication, selection and gene conversion in a Drosophila mojavensis female reproductive protein family. Genetics 181, 1451–1465 (doi:10.1534/genetics.108.099044)

    Not in our library10.1534/genetics.108.099044

  138. 138.

    Beckmann J. S. Estivill X. Antonarakis S. E. 2007 Copy number variants and genetic traits: closer to the resolution of phenotypic to genotypic variability. Nat. Rev. Genet. 8, 639–646 (doi:10.1038/nrg2149)

    Not in our library10.1038/nrg2149

  139. 139.

    Andolfatto P. 2005 Adaptive evolution of non-coding DNA in Drosophila. Nature 437, 1149–1152 (doi:10.1038/nature04107)

    Not in our library10.1038/nature04107

  140. 140.

    Bergthorsson U. Andersson D. I. Roth J. R. 2007 Ohno's dilemma: evolution of new genes under continuous selection. Proc. Natl Acad. Sci. USA 104, 17 004–17 009 (doi:10.1073/pnas.0707158104)

    Not in our library10.1073/pnas.0707158104

  141. 141.

    Andersson D. I. Hughes D. 2009 Gene amplification and adaptive evolution in bacteria. Annu. Rev. Genet. 43, 167–195 (doi:10.1146/annurev-genet-102108-134805)

    Not in our library10.1146/annurev-genet-102108-134805

  142. 142.

    Levasseur A. Pontarotti P. 2011 The role of duplications in the evolution of genomes highlights the need for evolutionary-based approaches in comparative genomics. Biol. Direct. 6, 11 (doi:10.1186/1745-6150-6-11)

    Not in our library10.1186/1745-6150-6-11

  143. 143.

    Holloway A. K. Palzkill T. Bull J. J. 2007 Experimental evolution of gene duplicates in a bacterial plasmid model. J. Mol. Evol. 64, 215–222 (doi:10.1007/s00239-006-0087-x)

    Not in our library10.1007/s00239-006-0087-x

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    Reams A. B. Kofoid E. Savageau M. Roth J. R. 2010 Duplication frequency in a population of Salmonella enterica rapidly approaches steady state with or without recombination. Genetics 184, 1077–1094 (doi:10.1534/genetics.109.111963)

    Not in our library10.1534/genetics.109.111963

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