Genome biology Journal Impact Factor & Information

Publisher: BioMed Central

Journal description

Genome Biology publishes articles from the full spectrum of biology. Subjects covered include any aspect of molecular, cellular, organismal or population biology studied from a genomic perspective, as well as genomics, proteomics, bioinformatics, genomic methods (including structure prediction), computational biology, sequence analysis (including large-scale and cross-genome analyses), comparative biology and evolution.

Current impact factor: 10.81

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 10.81
2013 Impact Factor 10.465
2012 Impact Factor 10.288
2011 Impact Factor 9.036
2010 Impact Factor 6.885

Impact factor over time

Impact factor

Additional details

5-year impact 13.48
Cited half-life 6.00
Immediacy index 1.94
Eigenfactor 0.09
Article influence 6.86
Website Genome Biology website
Other titles Genome biology (Online), Genome biology,, GB. C
ISSN 1465-6914
OCLC 49210873
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

BioMed Central

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Publisher's version/PDF may be used
    • Eligible UK authors may deposit in OpenDepot
    • Creative Commons Attribution License
    • Copy of License must accompany any deposit.
    • All titles are open access journals
    • 'BioMed Central' is an imprint of 'Springer Verlag (Germany)'
  • Classification

Publications in this journal

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    [Show abstract] [Hide abstract]
    ABSTRACT: A recent study finds that changes to transcription and DNA methylation resulting from in utero exposure to environmental endocrine-disrupting chemicals are not inherited across generations.
    Genome biology 12/2015; 16(1):60. DOI:10.1186/s13059-015-0626-0
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    ABSTRACT: Average genome size is an important, yet often overlooked, property of microbial communities. We developed MicrobeCensus to rapidly and accurately estimate average genome size from shotgun metagenomic data and applied our tool to 1,352 human microbiome samples. We found that average genome size differs significantly within and between body sites and tracks with major functional and taxonomic differences. In the gut, average genome size is positively correlated with the abundance of Bacteroides and genes related to carbohydrate metabolism. Importantly, we found that average genome size variation can bias comparative analyses, and that normalization improves detection of differentially abundant genes. Electronic supplementary material The online version of this article (doi:10.1186/s13059-015-0611-7) contains supplementary material, which is available to authorized users.
    Genome biology 12/2015; 16(1):51. DOI:10.1186/s13059-015-0611-7
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    ABSTRACT: The spliceosome is a huge molecular machine that assembles dynamically onto its pre-mRNA substrates. A new study based on interactome analysis provides clues about how splicing-regulatory proteins modulate assembly of the spliceosome to either activate or repress splicing. Please see related Research article:
    Genome biology 07/2015; 16(1):135. DOI:10.1186/s13059-015-0707-0
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    ABSTRACT: One of the most important recent findings in cancer genomics is the identification of novel driver mutations which often target genes that regulate genome-wide chromatin and DNA methylation marks. Little is known, however, as to whether these genes exhibit patterns of epigenomic deregulation that transcend cancer types. Here we conduct an integrative pan-cancer-wide analysis of matched RNA-Seq and DNA methylation data across ten different cancer types. We identify seven tumor suppressor and eleven oncogenic epigenetic enzymes which display patterns of deregulation and association with genome-wide cancer DNA methylation patterns, which are largely independent of cancer type. In doing so, we provide evidence that genome-wide cancer hyper- and hypo- DNA methylation patterns are independent processes, controlled by distinct sets of epigenetic enzyme genes. Using causal network modeling, we predict a number of candidate drivers of cancer DNA hypermethylation and hypomethylation. Finally, we show that the genomic loci whose DNA methylation levels associate most strongly with expression of these putative drivers are highly consistent across cancer types. This study demonstrates that there exist universal patterns of epigenomic deregulation that transcend cancer types, and that intra-tumor levels of genome-wide DNA hypomethylation and hypermethylation are controlled by distinct processes.
    Genome biology 07/2015; 16(1):140. DOI:10.1186/s13059-015-0699-9
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    ABSTRACT: Long non-coding RNAs (lncRNAs) are not translated into proteins and were initially considered to be part of the 'dark matter' of the genome. Recently, it has been shown that lncRNAs play a role in the recruitment of chromatin modifying complexes and can influence gene expression. However, it is unknown if lncRNAs function in a similar way in cancer. Here, we show that the lncRNA ROR occupies and activates the TESC promoter by repelling the histone G9A methyltransferase and promoting the release of histone H3K9 methylation. Suppression of ROR in tumors results in silencing of TESC expression, and G9A-mediated histone H3K9 methylation in the TESC promoter is restored, which significantly reduces tumor growth and metastasis. Without ROR silencing, TESC knockdown presents consistent and significant reductions in tumor progression. Our results reveal a novel mechanism by which ROR may serve as a decoy oncoRNA that blocks binding surfaces, preventing the recruitment of histone modifying enzymes, thereby specifying a new pattern of histone modifications that promote tumorigenesis.
    Genome biology 07/2015; 16(1):139. DOI:10.1186/s13059-015-0705-2
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    ABSTRACT: Exitrons are exon-like introns located within protein-coding exons. Removal or retention of exitrons through alternative splicing increases proteome complexity and thus adds to phenotypic diversity.
    Genome biology 07/2015; 16(1):136. DOI:10.1186/s13059-015-0704-3
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    ABSTRACT: The initial next-generation sequencing technologies produced reads of 25 or 36 bp, and only from a single-end of the library sequence. Currently, it is possible to reliably produce 300 bp paired-end sequences for RNA expression analysis. While read lengths have consistently increased, people have assumed that longer reads are more informative and that paired-end reads produce better results than single-end reads. We used paired-end 101 bp reads and trimmed them to simulate different read lengths, and also separated the pairs to produce single-end reads. For each read-length and paired status, we evaluated differential expression levels between two standard samples and compared the results to those obtained by qPCR. We found that, with the exception of 25 bp reads, there is little difference for the detection of differential expression regardless of the read length. Once single-end reads are at a length of 50 bp, the results do not change substantially for any level up to, and including, 100 bp paired-end. However, splice junction detection significantly improves as the read length increases with 100 bp paired-end showing the best performance. We performed the same analysis on two ENCODE samples and found consistent results confirming that our conclusions have broad application. A researcher could save substantial resources by using 50 bp single-end reads for differential expression analysis instead of using longer reads. However, splicing detection is unquestionably improved by paired-end and longer reads. Therefore, an appropriate read length should be used based on the final goal of the study.
    Genome biology 06/2015; 16(1):131. DOI:10.1186/s13059-015-0697-y
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    ABSTRACT: The Forkhead (FKH) transcription factor FOXM1 is a key regulator of the cell cycle and is overexpressed in most types of cancer. FOXM1, similar to other FKH factors, binds to a canonical FKH motif in vitro. However, genome-wide mapping studies in different cell lines have shown a lack of enrichment of the FKH motif, suggesting an alternative mode of chromatin recruitment. We have investigated the role of direct versus indirect DNA binding in FOXM1 recruitment by performing ChIP-seq with wild-type and DNA binding deficient FOXM1. An in vitro fluorescence polarization assay identified point mutations in the DNA binding domain of FOXM1 that inhibit binding to a FKH consensus sequence. Cell lines expressing either wild-type or DNA binding deficient GFP-tagged FOXM1 were used for genome-wide mapping studies comparing the distribution of the DNA binding deficient protein to the wild-type. This shows that interaction of the FOXM1 DNA binding domain with target DNA is essential for recruitment. Moreover, analysis of the protein interactome of wild-type versus DNA binding deficient FOXM1 shows that the reduced recruitment is not due to inhibition of protein-protein interactions. A functional DNA binding domain is essential for FOXM1 chromatin recruitment. Even in FOXM1 mutants with almost complete loss of binding, the protein-protein interactions and pattern of phosphorylation are largely unaffected. These results strongly support a model whereby FOXM1 is specifically recruited to chromatin through co-factor interactions by binding directly to non-canonical DNA sequences.
    Genome biology 06/2015; 16(1):130. DOI:10.1186/s13059-015-0696-z
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    ABSTRACT: An innovative, microwell-based platform for single-cell RNA sequencing (RNA-seq) combines cost efficiency, scalability and parallelizability, and will enable many new avenues of biological inquiry. See related Research article:
    Genome biology 06/2015; 16(1):129. DOI:10.1186/s13059-015-0695-0
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    ABSTRACT: A new study provides evidence that gene transposition from sex chromosomes to autosomes is a conserved phenomenon across mammalian species that rescues dosage-sensitive genes.
    Genome biology 06/2015; 16(1):121. DOI:10.1186/s13059-015-0686-1