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 (OUP)

Journal 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.

Current impact factor: 9.11

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 9.105
2013 Impact Factor 14.308
2012 Impact Factor 10.353
2011 Impact Factor 5.55
2010 Impact Factor 5.51
2009 Impact Factor 9.872
2008 Impact Factor 7.28
2007 Impact Factor 6.438
2006 Impact Factor 6.726
2005 Impact Factor 6.233
2004 Impact Factor 6.355
2003 Impact Factor 6.05
2002 Impact Factor 5.271
2001 Impact Factor 5.357
2000 Impact Factor 5.298
1999 Impact Factor 4.983
1998 Impact Factor 5.291
1997 Impact Factor 5.249
1996 Impact Factor 5.969
1995 Impact Factor 5.399
1994 Impact Factor 5.024
1993 Impact Factor 3.902
1992 Impact Factor 3.737

Impact factor over time

Impact factor
Year

Additional details

5-year impact 11.67
Cited half-life 7.10
Immediacy index 1.75
Eigenfactor 0.09
Article influence 4.44
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 (OUP)

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Pre-print can only be posted prior to acceptance
    • Pre-print on pre-print servers
    • Pre-prints that are accepted will be required to select Oxford Open when accepted
    • Pre-print must be accompanied by set statement (see link) and state of article review
    • Pre-print must match current version under consideration
    • Pre-print must be ammended with a a link to published version
    • Post-print in Institutional repositories or Central repositories
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany archived copy (see policy)
    • Eligible authors may deposit in OpenDepot
    • The publisher will deposit in PubMed Central on behalf of NIH authors
    • This policy is an exception to the default policies of 'Oxford University Press (OUP)'
  • Classification
    yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The p53 tumor suppressor and its key regulator MDM2 play essential roles in development, ageing, cancer and cellular stress responses in mammals. Following DNA damage, MDM2 interacts with p53 mRNA in an ATM kinase-dependent fashion and stimulates p53 synthesis whereas under normal conditions MDM2 targets the p53 protein for degradation. The peptide- and RNA-motifs that interact with MDM2 are encoded by the same conserved BOX-I sequence but how these interactions have evolved is unknown. Here we show that a temperature-sensitive structure in the invertebrate Ciona intestinalis (Ci) p53 mRNA controls its interaction with MDM2. We also show that a non-conserved flanking region of Ci-BOX-I domain prevents the p53-MDM2 protein-protein interaction. These results indicate that the temperature-regulated p53 mRNA–MDM2 interaction evolved to become kinase-regulated in the mammalian DNA damage response. The data also suggest that the negative regulation of p53 by MDM2 via protein–protein interaction evolved in vertebrates following changes in the BOX-I flanking sequence.
    No preview · Article · Jan 2016 · Molecular Biology and Evolution
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    ABSTRACT: Genetic differentiation across populations that is maintained in the presence of gene flow is a hallmark of spatially varying selection. In Drosophila melanogaster, the latitudinal clines across the eastern coasts of Australia and North America appear to be examples of this type of selection, with recent studies showing that a substantial portion of the D. melanogaster genome exhibits allele frequency differentiation with respect to latitude on both continents. As of yet there has been no genome-wide examination of differentiated copy-number variants (CNVs) in these geographic regions, despite their potential importance for phenotypic variation in Drosophila and other taxa. Here, we present an analysis of geographic variation in CNVs in D. melanogaster. We also present the first genomic analysis of geographic variation for copy-number variation in the sister species, D. simulans, in order to investigate patterns of parallel evolution in these close relatives. In D. melanogaster we find hundreds of CNVs, many of which show parallel patterns of geographic variation on both continents, lending support to the idea that they are influenced by spatially varying selection. These findings support the idea that polymorphic CNVs contribute to local adaptation in D. melanogaster. In contrast, we find very few CNVs in D. simulans that are geographically differentiated in parallel on both continents, consistent with earlier work suggesting that clinal patterns are weaker in this species.
    No preview · Article · Jan 2016 · Molecular Biology and Evolution
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    ABSTRACT: B cell receptors (BCRs) are membrane-bound immunoglobulins that recognize and bind foreign proteins (antigens). BCRs are formed through random somatic changes of germline DNA, creating a vast repertoire of unique sequences that enable individuals to recognise a diverse range of antigens. After encountering antigen for the first time, BCRs undergo a process of affinity maturation, whereby cycles of rapid somatic mutation and selection lead to improved antigen binding. This constitutes an accelerated evolutionary process that takes place over days or weeks. Next-generation sequencing of the gene regions that determine BCR binding has begun to reveal the diversity and dynamics of BCR repertoires in unprecedented detail. Although this new type of sequence data has the potential to revolutionise our understanding of infection dynamics, quantitative analysis is complicated by the unique biology and high diversity of BCR sequences. Models and concepts from molecular evolution and phylogenetics that have been applied successfully to rapidly evolving pathogen populations are increasingly being adopted to study BCR diversity and divergence within individuals. However, BCR dynamics may violate key assumptions of many standard evolutionary methods, as they do not descend from a single ancestor, and experience biased mutation. Here we review the application of evolutionary models to BCR repertoires and discuss the issues we believe need be addressed for this inter-disciplinary field to flourish.
    Full-text · Article · Jan 2016 · Molecular Biology and Evolution
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    ABSTRACT: Heritable differences in gene expression are caused by mutations in DNA sequences encoding cis-regulatory elements and trans-regulatory factors. These two classes of regulatory change differ in their relative contributions to expression differences in natural populations and are the result of the combined effects of mutation and natural selection. Here, we investigate how new mutations create the regulatory variation upon which natural selection acts by quantifying the frequencies and effects of hundreds of new cis- and trans-acting mutations altering activity of the TDH3 promoter in the yeast Saccharomyces cerevisiae in the absence of natural selection. We find that cis-regulatory mutations have larger effects on expression than trans-regulatory mutations and that while trans-regulatory mutations are more common overall, cis- and trans-regulatory changes in expression are equally abundant when only the largest changes in expression are considered. In addition, we find that cis-regulatory mutations are skewed towards decreased expression while trans-regulatory mutations are skewed towards increased expression. We also measure the effects of cis- and trans-regulatory mutations on the variability in gene expression among genetically identical cells, a property of gene expression known as expression noise, finding that trans-regulatory mutations are much more likely to decrease expression noise than cis-regulatory mutations. Because new mutations are the raw material upon which natural selection acts, these differences in the frequencies and effects of cis- and trans-regulatory mutations should be considered when creating models of regulatory evolution.
    No preview · Article · Jan 2016 · Molecular Biology and Evolution
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    ABSTRACT: Qualitative patterns of gene activation and repression are often conserved despite an abundance of quantitative variation in expression levels within and between species. A major challenge to interpreting patterns of expression divergence is knowing which changes in gene expression affect fitness. To characterize the fitness effects of gene expression divergence we placed orthologous promoters from eight yeast species upstream of malate synthase (MLS1) in Saccharomyces cerevisiae. As expected, we found these promoters varied in their expression level under activated and repressed conditions as well as in their dynamic response following loss of glucose repression. Despite these differences, only a single promoter driving near basal levels of expression caused a detectable loss of fitness. We conclude that the MLS1 promoter lies on a fitness plateau whereby even large changes in gene expression can be tolerated without a substantial loss of fitness.
    Full-text · Article · Jan 2016 · Molecular Biology and Evolution
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    ABSTRACT: The source of genetic novelty is an area of wide interest and intense investigation. Although gene duplication is conventionally thought to dominate the production of new genes, this view was recently challenged by a proposal of widespread de novo gene origination in eukaryotic evolution. Specifically, distributions of various gene properties such as coding sequence length, expression level, codon usage, and probability of being subject to purifying selection among groups of genes with different estimated ages were reported to support a model in which new protein-coding proto-genes arise from noncoding DNA and gradually integrate into cellular networks. Here we show that the genomic patterns asserted to support widespread de novo gene origination are largely attributable to biases in gene age estimation by phylostratigraphy, because such patterns are also observed in phylostratigraphic analysis of simulated genes bearing identical ages. Furthermore, there is no evidence of purifying selection on very young de novo genes previously claimed to show such signals. Together, these findings are consistent with the prevailing view that de novo gene birth is a relatively minor contributor to new genes in genome evolution. They also illustrate the danger of using phylostratigraphy in the study of new gene origination without considering its inherent bias.
    No preview · Article · Jan 2016 · Molecular Biology and Evolution
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    Preview · Article · Jan 2016 · Molecular Biology and Evolution
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    Preview · Article · Dec 2015 · Molecular Biology and Evolution
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    Preview · Article · Dec 2015 · Molecular Biology and Evolution
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    Preview · Article · Dec 2015 · Molecular Biology and Evolution
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    ABSTRACT: We present three linkage-disequilibrium (LD)-based recombination maps generated using whole-genome sequence data from 10 Nigerian chimpanzees, 13 bonobos, and 15 western gorillas, collected as part of the Great Ape Genome Project (Prado-Martinez, et al. 2013). We also identified species-specific recombination hotspots in each group using a modified LDhot framework, which greatly improves statistical power to detect hotspots at varying strengths. We show that fewer hotspots are shared among chimpanzee subspecies than within human populations, further narrowing the time-scale of complete hotspot turnover. Further, using species-specific PRDM9 sequences to predict potential binding sites, we show higher predicted PRDM9 binding in recombination hotspots as compared to matched cold spot regions in multiple great ape species, including at least one chimpanzee subspecies. We found that correlations between broad-scale recombination rates decline more rapidly than nucleotide divergence between species. We also compared the skew of recombination rates at centromeres and telomeres between species and show a skew from chromosome means extending as far as 10-15 Mb from chromosome ends. Further, we examined broad-scale recombination rate changes near a translocation in gorillas and found minimal differences as compared to other great ape species perhaps because the coordinates relative to the chromosome ends were unaffected. Finally, based on multiple linear regression analysis, we found that various correlates of recombination rate persist throughout the African great apes including repeats, diversity, and divergence. Our study is the first to analyze within- and between-species genome-wide recombination rate variation in several close relatives.
    No preview · Article · Dec 2015 · Molecular Biology and Evolution