Molecular Biology and Evolution (MOL BIOL EVOL )

Publisher: Molecular Biology and Evolution Society; American Society of Naturalists; Society for the Study of Evolution, Oxford University Press

Description

Molecular Biology and Evolution (MBE) is devoted to the interdisciplinary science between molecular biology and evolutionary biology. MBE emphasizes experimental papers, but theoretical papers are also published if they have a solid biological basis. Although this journal is primarily for original papers, review articles and book reviews are also published. MBE is an appropriate outlet for the examination of molecular evolutionary processes and patterns, and the testing of evolutionary hypotheses with molecular data. MBE is not an appropriate outlet for purely taxonomic treatments and the detailing of systematic issues. Published by the Society for Molecular Biology and Evolution.

  • Impact factor
    14.31
    Hide impact factor history
     
    Impact factor
  • 5-year impact
    11.22
  • Cited half-life
    6.30
  • Immediacy index
    1.56
  • Eigenfactor
    0.10
  • Article influence
    4.05
  • Website
    Molecular Biology and Evolution website
  • Other titles
    Molecular biology and evolution, MBE
  • ISSN
    0737-4038
  • OCLC
    9364605
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Oxford University Press

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo on science, technology, medicine articles
    • 2 years embargo on arts and humanities articles
    • Some titles may have different embargoes
  • Conditions
    • Pre-print can only be posted prior to acceptance
    • Pre-print must be accompanied by set statement (see link)
    • Pre-print must not be replaced with post-print, instead a link to published version with amended set statement should be made
    • Pre-print on author's personal website, employer website, free public server or pre-prints in subject area
    • Post-print in Institutional repositories or Central repositories
    • Publisher version cannot be used except for Nucleic Acids Research articles
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany archived copy (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
    • Eligible UK authors may deposit in OpenDepot
    • Publisher will deposit on behalf of NIH funded authors to PubMed Central, Nucleic Acids Research authors must pay their fee first
    • Some titles may use different policies
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Dimorphic mating-type chromosomes in fungi are excellent models for understanding the genomic consequences of recombination suppression. Their suppressed recombination and reduced effective population size are expected to limit the efficacy of natural selection, leading to genomic degeneration. Our aim was to identify the sequences of the mating-type chromosomes (a1 and a2) of the anther smut fungi and to investigate degeneration in their non-recombining regions. We used the haploid a1 Microbotryum lychnidis-dioicae reference genome sequence. The a1 and a2 mating-type chromosomes were both isolated electrophoretically and sequenced. Integration with restriction-digest optical maps identified regions of recombination and non-recombination in the mating-type chromosomes. Genome sequence data was also obtained for twelve other Microbotryum species. We found strong evidence of degeneration across the genus in the non-recombining regions of the mating-type chromosomes, with significantly higher rates of non-synonymous substitution (dN/dS) than in non-mating-type chromosomes or in recombining regions of the mating-type chromosomes. The non-recombining regions of the mating-type chromosomes also showed high transposable element content, weak gene expression and gene losses. The levels of degeneration did not differ between the a1 and a2 mating-type chromosomes, consistent with the lack of homogametic/heterogametic asymmetry between them, and contrasting with X/Y or Z/W sex chromosomes.
    Molecular Biology and Evolution 12/2014;
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    ABSTRACT: Allopolyploidization in plants entails the merger of two divergent nuclear genomes, typically with only one set (usually maternal) of parental plastidial and mitochondrial genomes and with an altered cytonuclear stoichiometry. Thus, we might expect cytonuclear coevolution to be an important dimension of allopolyploid evolution. Here we investigate cytonuclear coordination for the key chloroplast protein rubisco (ribulose 1,5-bisphosphate carboxylase/oxygenase), which is composed of nuclear-encoded, small subunits (SSUs) and plastid-encoded, large subunits (LSUs). By studying gene composition and diversity as well as gene expression in four model allopolyploid lineages, Arabidopsis, Arachis, Brassica, and Nicotiana, we demonstrate that paralogous nuclear-encoded rbcS genes within diploids are subject to homogenization via gene conversion, and that such concerted evolution via gene conversion characterizes duplicated genes (homoeologs) at the polyploid level. Many gene conversions in the polyploids are inter-genomic with respect to the diploid progenitor genomes, occur in functional domains of the homoeologous SSUs, and are directionally biased such that the maternal amino acid states are favored. This consistent preferential maternal-to-paternal gene conversion is mirrored at the transcriptional level, with a uniform transcriptional bias of the maternal-like rbcS homoeologs. These data, repeated among multiple diverse angiosperm genera for an important photosynthetic enzyme, suggest that cytonuclear coevolution may be mediated by inter-genomic gene conversion and altered transcription of duplicated, now homoeologous nuclear genes.
    Molecular Biology and Evolution 07/2014;
  • Molecular Biology and Evolution 07/2014;
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    ABSTRACT: The endosymbiotic bacteria Wolbachia pipientis is known to infect a wide range of arthropod species yet less is known about the coevolutionary history it has with its hosts. Evidence of highly identical W. pipientis strains in evolutionary divergent hosts suggests horizontal transfer between hosts. For example, Drosophila ananassae is infected with a W. pipientis strain that is nearly identical in sequence to a strain that infects both D. simulans and D. suzukii, suggesting recent horizontal transfer among these three species. However, it is unknown whether the W. pipientis strain had recently invaded all three species or a more complex infectious dynamic underlies the horizontal transfers. Here we have examined the coevolutionary history of D. ananassae and its resident W. pipientis to infer its period of infection. Phylogenetic analysis of D. ananassae mitochondrial DNA and W. pipientis DNA sequence diversity revealed the current W. pipientis infection is not recent. In addition, we examined the population genetics and molecular evolution of several Germline Stem Cell (GSC) regulating genes of D. ananassae. These studies reveal significant evidence of recent and long-term positive selection at stonewall in D. ananassae, while pumillio showed patterns of variation consistent with only recent positive selection. Previous studies had found evidence for adaptive evolution of two key germline differentiation genes, bag of marbles (bam) and benign gonial cell neoplasm (bgcn), in D. melanogaster and D. simulans and proposed that the adaptive evolution at these two genes was driven by arms race between the host GSC and W. pipientis. However, we did not find any statistical departures from a neutral model of evolution for bam and bgcn in D. ananassae despite our new evidence that this species has been infected with W. pipientis for a period longer than the most recent infection in D. melanogaster. In the end analyzing the GSC regulating genes individually showed two out of the seven genes to have evidence of selection. However, combining the dataset and fitting a specific population genetic model significant proportion of the nonsynonymous sites across the GSC regulating genes were driven to fixation by positive selection. Clearly the GSC system is under rapid evolution and potentially multiple drivers are causing the rapid evolution.
    Molecular Biology and Evolution 06/2014;
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    ABSTRACT: Scientists are assembling sequence data sets from increasing numbers of species and genes to build comprehensive timetrees. However, data are often unavailable for some species and gene combinations, and the proportion of missing data is often large for data sets containing many genes and species. Surprisingly, there has not been a systematic analysis of the effect of the degree of sparseness of the species-gene matrix on the accuracy of divergence time estimates. Here, we present results from computer simulations and empirical data analyses to quantify the impact of missing gene data on divergence time estimation in large phylogenies. We found that estimates of divergence times were robust even when sequences from a majority of genes for most of the species were absent. From the analysis of such extremely sparse data sets, we found that the most egregious errors occurred for nodes in the tree that had no common genes for any pair of species in the immediate descendant clades of the node in question. These problematic nodes can be easily detected prior to computational analyses based only on the input sequence alignment and the tree topology. We conclude that it is best to use larger alignments, since adding both genes and species to the alignment augments the number of genes available for estimating divergence events deep in the tree, and improves their time estimates.
    Molecular Biology and Evolution 06/2014;
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    ABSTRACT: Echolocation is a sensory system whereby certain mammals navigate and forage using sound waves, usually in environments where visibility is limited. Curiously, echolocation has evolved independently in bats and whales, which occupy entirely different environments. Based on this phenotypic convergence, recent studies identified several echolocation-related genes with parallel sites at the protein sequence level among different echolocating mammals, and among these, prestin seems the most promising. Although previous studies analyzed the evolutionary mechanism of prestin, the functional roles of the parallel sites in the evolution of mammalian echolocation are not clear. By functional assays, we show that a key parameter of prestin function, 1/α, is increased in all echolocating mammals and that the N7T parallel substitution accounted for this functional convergence. Moreover, another parameter, V1/2, was shifted toward the depolarization direction in a toothed whale, the bottlenose dolphin (Tursiops truncatus) and a constant-frequency bat, Stoliczka's trident bat (Aselliscus stoliczkanus). The parallel site of I384T between toothed whales and constant-frequency (CF) bats was responsible for this functional convergence. Furthermore, the two parameters (1/α and V1/2) were correlated with mammalian high-frequency hearing, suggesting that the convergent changes of the prestin function in echolocating mammals may play important roles in mammalian echolocation. To our knowledge, these findings present the functional patterns of echolocation-related genes in echolocating mammals for the first time and rigorously demonstrate adaptive parallel evolution at the protein sequence level, paving the way to insights into the molecular mechanism underlying mammalian echolocation.
    Molecular Biology and Evolution 06/2014;
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    ABSTRACT: Plastids utilise a complex gene expression machinery, which has coevolved with the underlying genome sequence. Relatively little is known about the genome-wide evolution of transcript processing in algal plastids that have undergone complex endosymbiotic events. We present the first genome-wide study of transcript processing in a plastid acquired through serial endosymbiosis, in the fucoxanthin-containing dinoflagellate Karlodinium veneficum. The fucoxanthin dinoflagellate plastid has an extremely divergent genome, and utilises two unusual transcript processing pathways, 3' poly(U) tail addition, and sequence editing, which were acquired following the serial endosymbiosis event. We demonstrate that poly(U) addition and sequence editing are widespread features across the K. veneficum plastid transcriptome, whereas other dinoflagellate plastid lineages that have arisen through independent serial endosymbiosis events do not utilise either RNA processing pathway. These pathways constrain the effects of divergent sequence evolution in fucoxanthin plastids, for example by correcting mutations in the genomic sequence that would otherwise be deleterious, and are specifically associated with transcripts that encode functional plastid proteins over transcripts of recently generated pseudogenes. These pathways may have additionally facilitated divergent evolution within the K. veneficum plastid. Transcript editing, for example, has contributed to the evolution of a novel C-terminal sequence extension on the K. veneficum AtpA protein. We furthermore provide the first complete sequence of an episomal minicircle in a fucoxanthin dinoflagellate plastid, which contains the dnaK gene, and gives rise to polyuridylylated and edited transcripts. Our results indicate that RNA processing in fucoxanthin dinoflagellate plastids is evolutionarily dynamic, coevolving with the underlying genome sequence.
    Molecular Biology and Evolution 06/2014;
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    ABSTRACT: For sequences that are highly divergent, there is often insufficient information to infer accurate alignments, and phylogenetic uncertainty may be high. One way to address this issue is to make use of protein structural information, since structures generally diverge more slowly than sequences. In this work, we extend a recently developed stochastic model of pairwise structural evolution to multiple structures on a tree, analytically integrating over ancestral structures to permit efficient likelihood computations under the resulting joint sequence-structure model. We observe that the inclusion of structural information significantly reduces alignment and topology uncertainty, and reduces the number of topology and alignment errors in cases where the true trees and alignments are known. In some cases the inclusion of structure results in changes to the consensus topology, indicating that structure may contain additional information beyond that which can be obtained from sequences. We use the model to investigate the order of divergence of cytoglobins, myoglobins, and haemoglobins, and observe a stabilisation of phylogenetic inference: while a sequence-based inference assigns significant posterior probability to several different topologies, the structural model strongly favours one of these over the others, and is more robust to the choice of dataset.
    Molecular Biology and Evolution 06/2014;
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    ABSTRACT: Cells govern biological functions through complex biological networks. Perturbations to networks may drive cells to new phenotypic states, e.g., tumorigenesis. Identifying how genetic lesions perturb molecular networks is a fundamental challenge. This study used large-scale human interactome data to systematically explore the relationship among network topology, somatic mutation, evolutionary rate, and evolutionary origin of cancer genes. We found the unique network centrality of cancer proteins, which is largely independent of gene essentiality. Cancer genes likely have experienced a lower evolutionary rate and stronger purifying selection compared to non-cancer genes, Mendelian and orphan disease genes. Cancer proteins tend to have ancient histories, likely originated in early metazoan, although they are younger than proteins encoded by Mendelian disease genes, orphan disease genes, and essential genes. We found that the protein evolutionary origin (age) positively correlates with protein connectivity in the human interactome. Furthermore, we investigated the network-attacking perturbations due to somatic mutations identified from 3,268 tumors across 12 cancer types in The Cancer Genome Atlas. We observed a positive correlation between protein connectivity and the number of nonsynonymous somatic mutations, while a weaker or insignificant correlation between protein connectivity and the number of synonymous somatic mutations. These observations suggest that somatic mutational network-attacking perturbations to hub genes play an important role in tumor emergence and evolution. Collectively, this work has broad biomedical implications for both basic cancer biology and the development of personalized cancer therapy.
    Molecular Biology and Evolution 05/2014;
  • Molecular Biology and Evolution 05/2014;
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    ABSTRACT: Current estimates of diversifying positive selection rely on first having an accurate multiple sequence alignment. Simulation studies have shown that under biologically plausible conditions, relying on a single estimate of the alignment from commonly used alignment software can lead to unacceptably high false positive rates in detecting diversifying positive selection. We present a novel statistical method that eliminates excess false positives resulting from alignment error by jointly estimating the degree of positive selection and the alignment under an evolutionary model. Our model treats both substitutions and insertions/deletions as sequence changes on a tree, and allows site-heterogeneity in the substitution process. We conduct inference starting from unaligned sequence data by integrating over all alignments. This approach naturally accounts for ambiguous alignments without requiring ambiguously aligned sites to be identified and removed prior to analysis. We take a Bayesian approach and conduct inference using MCMC to integrate over all alignments on a fixed evolutionary tree topology. We introduce a Bayesian version of the branch-site test and assess the evidence for positive selection using Bayes factors. We compare two models of differing dimensionality using a simple alternative to reversible-jump methods. We also describe a more accurate method of estimating the Bayes factor using Rao-Blackwellization. We then show using simulated data that jointly estimating the alignment and the presence of positive selection solves the problem with excessive false positives from erroneous alignments, and has nearly the same power to detect positive selection as when the true alignment is known. We also show that samples taken from the posterior alignment distribution using the software BAli-Phy have substantially lower alignment error compared to MUSCLE, MAFFT, PRANK, and FSA alignments.
    Molecular Biology and Evolution 05/2014;