Trends in Genetics (TRENDS GENET)

Publisher: Elsevier

Journal description

Now the highest-cited journal in Genetics. (ISI/SCI Journal Citation Reports 11.313.1998). Multi-faceted and highly-cited, from developmental biology to genomics. Each monthly issue contains concise, lively and up-to-date Reviews as well as a section for Comment on the latest developments, a journal monitoring feature, Genetwork (a column about Internet resources), Meeting Reports, and Book, Software and CD-ROM reviews, and new in 98 - genetics and society. Most articles are commissioned, and all review articles are peer-reviewed. Trends in Genetics' prestigious Editorial Board attests to the journal's established reputation as essential reading for all those interested in the molecular themes of genetics, differentiation and development. Trends in Genetics' readers use the journal to keep up with the latest developments in both their own and related fields, and as a valuable resource for teaching.

Current impact factor: 9.92

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 9.918
2013 Impact Factor 11.597
2012 Impact Factor 9.772
2011 Impact Factor 10.064
2010 Impact Factor 11.364
2009 Impact Factor 8.689
2008 Impact Factor 8.659
2007 Impact Factor 9.729
2006 Impact Factor 9.95
2005 Impact Factor 12.047
2004 Impact Factor 14.643
2003 Impact Factor 12.016
2002 Impact Factor 13.216
2001 Impact Factor 12.417
2000 Impact Factor 12.912
1999 Impact Factor 16.342
1998 Impact Factor 11.313
1997 Impact Factor 9.978
1996 Impact Factor 10.781
1995 Impact Factor 10.446
1994 Impact Factor 10.11
1993 Impact Factor 9.976
1992 Impact Factor 11.497

Impact factor over time

Impact factor

Additional details

5-year impact 9.86
Cited half-life 8.90
Immediacy index 2.16
Eigenfactor 0.03
Article influence 4.82
Website Trends in Genetics website
Other titles Trends in genetics, Genetics, TIG, Trends in biochemical sciences., Trends in cell biology
ISSN 0168-9525
OCLC 11747206
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On non-commercial hosting platforms including institutional repository
    • Published source must be acknowledged
    • Must link to journal homepage with DOI
    • Publisher's version/PDF cannot be used
    • Publisher last reviewed on 05/08/2015
    • 'Elsevier (Cell Press)' is an imprint of 'Elsevier'
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Host-pathogen interactions provide valuable systems for the study of evolutionary genetics and natural selection. The sequestration of essential iron has emerged as a crucial innate defense system termed nutritional immunity, leading pathogens to evolve mechanisms of 'iron piracy' to scavenge this metal from host proteins. This battle for iron carries numerous consequences not only for host-pathogen evolution but also microbial community interactions. Here we highlight recent and potential future areas of investigation on the evolutionary implications of microbial iron piracy in relation to molecular arms races, host range, competition, and virulence. Applying evolutionary genetic approaches to the study of microbial iron acquisition could also provide new inroads for understanding and combating infectious disease.
    Trends in Genetics 10/2015; DOI:10.1016/j.tig.2015.09.001
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    ABSTRACT: Pericentromeric DNA represents a large fraction of the mammalian genome that is usually assembled into heterochromatin. Recent advances have revealed that the composition of pericentromeric heterochromatin is surprisingly dynamic. Indeed, high levels of histone H3 trimethylation on lysine 9 (H3K9me3) and DNA methylation normally characterize the repressive environment of this region. However, in specific tissues and in cancer cells, Polycomb proteins can occupy pericentromeric heterochromatin and act as a molecular sink for transcriptional regulators. Restoring heterochromatin methylation marks could, thus, be an important way to bring back normal gene expression programs in disease. Here, I discuss the potential mechanisms by which Polycomb complexes are recruited to pericentromeric DNA.
    Trends in Genetics 10/2015; DOI:10.1016/j.tig.2015.09.003
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    ABSTRACT: Research into chromosome structure and organization is an old field that has seen some fascinating progress in recent years. Modern molecular methods that can describe the shape of chromosomes have begun to revolutionize our understanding of genome organization and the mechanisms that regulate gene activity. A picture is beginning to emerge of chromatin loops representing a widespread organizing principle of the chromatin fiber and the proteins cohesin and CCCTC-binding factor (CTCF) as key players anchoring such chromatin loops. Here we review our current understanding of the features of CTCF- and cohesin-mediated genome organization and how their evolution may have helped to shape genome structure.
    Trends in Genetics 10/2015; DOI:10.1016/j.tig.2015.09.004
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    ABSTRACT: CHARGE syndrome is a rare genetic syndrome characterised by a unique combination of multiple organ anomalies. Dominant loss-of-function mutations in the gene encoding chromodomain helicase DNA binding protein 7 (CHD7), which is an ATP-dependent chromatin remodeller, have been identified as the cause of CHARGE syndrome. Here, we review recent work aimed at understanding the mechanism of CHD7 function in normal and pathological states, highlighting results from biochemical and in vivo studies. The emerging picture from this work suggests that the mechanisms by which CHD7 fine-tunes gene expression are context specific, consistent with the pleiotropic nature of CHARGE syndrome.
    Trends in Genetics 09/2015; DOI:10.1016/j.tig.2015.05.009
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    ABSTRACT: The broad diversity of cell types within vertebrates arises from a unique genetic blueprint by combining intrinsic cellular information with developmental and other extrinsic signals. Lying at the interface between cellular signals and the DNA is the chromatin, a dynamic nucleoprotein complex that helps to mediate gene regulation. The most basic subunit of chromatin, the nucleosome, consists of DNA wrapped around histones, a set of proteins that play crucial roles as scaffolding molecules and regulators of gene expression. Growing evidence indicates that canonical histones are commonly replaced by protein variants before and during cellular transitions. We highlight exciting new results suggesting that histone variants are essential players in the control of cellular plasticity during development and in the adult nervous system. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 08/2015; 31(9). DOI:10.1016/j.tig.2015.07.005
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    ABSTRACT: Adaptive radiation is the rapid and extensive ecological diversification of an organismal lineage to generate both phenotypic disparity (divergence) and similarity (convergence). Demonstrating particularly clear evidence of the power of natural selection, adaptive radiations serve as outstanding systems for studying the mechanisms of evolution. We review how the first wave of genomic investigation across major archetypal adaptive radiations has started to shed light on the molecular basis of adaptive diversification. Notably, these efforts have not yet identified consistent features of genomic architecture that promote diversification. However, access to a pool of ancient adaptive variation via genetic exchange emerges as an important driver of adaptive radiation. We conclude by highlighting avenues for future research on adaptive radiations, including the discovery of 'adaptation genes' based on genome scans using replicate convergent populations. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 08/2015; 31(9). DOI:10.1016/j.tig.2015.07.002
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    ABSTRACT: Sixty years ago, the position of a gene on a chromosome was seen to be a major determinant of gene activity; however, position effects are rarely central to current discussions of gene expression. We describe a comprehensive and simplifying view of how position in 1D sequence and 3D nuclear space underlies expression. We suggest that apparently-different regulatory motifs including enhancers, silencers, insulators, barriers, and boundaries act similarly - they are active promoters that tether target genes close to, or distant from, appropriate transcription sites or 'factories'. We also suggest that any active transcription unit regulates the firing of its neighbors - and thus can be categorized as one or other type of motif; this is consistent with expression quantitative trait loci (eQTLs) being widely dispersed. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 08/2015; 31(9). DOI:10.1016/j.tig.2015.07.001
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    ABSTRACT: Chromosome structural variation (SV) is a normal part of variation in the human genome, but some classes of SV can cause neurodevelopmental disorders. Analysis of the DNA sequence at SV breakpoints can reveal mutational mechanisms and risk factors for chromosome rearrangement. Large-scale SV breakpoint studies have become possible recently owing to advances in next-generation sequencing (NGS) including whole-genome sequencing (WGS). These findings have shed light on complex forms of SV such as triplications, inverted duplications, insertional translocations, and chromothripsis. Sequence-level breakpoint data resolve SV structure and determine how genes are disrupted, fused, and/or misregulated by breakpoints. Recent improvements in breakpoint sequencing have also revealed non-allelic homologous recombination (NAHR) between paralogous long interspersed nuclear element (LINE) or human endogenous retrovirus (HERV) repeats as a cause of deletions, duplications, and translocations. This review covers the genomic organization of simple and complex constitutional SVs, as well as the molecular mechanisms of their formation. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 07/2015; DOI:10.1016/j.tig.2015.05.010
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    ABSTRACT: The 3D folding of the genome and its relation to fundamental processes such as gene regulation, replication, and segregation remains one of the most puzzling and exciting questions in genetics. In this review, we describe how the use of new technologies is starting to revolutionize the field of chromosome organization, and to shed light on the mechanisms of transcription, replication, and repair. In particular, we concentrate on recent studies using genome-wide methods, single-molecule technologies, and super-resolution microscopy (SRM). We summarize some of the main concerns when employing these techniques, and discuss potential new and exciting perspectives that illuminate the connection between 3D genomic organization and gene regulation. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 06/2015; 31(8). DOI:10.1016/j.tig.2015.05.011
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    ABSTRACT: Gene expression is precisely controlled in time and space through the integration of signals that act at gene promoters and gene-distal enhancers. Classically, promoters and enhancers are considered separate classes of regulatory elements, often distinguished by histone modifications. However, recent studies have revealed broad similarities between enhancers and promoters, blurring the distinction: active enhancers often initiate transcription, and some gene promoters have the potential to enhance transcriptional output of other promoters. Here, we propose a model in which promoters and enhancers are considered a single class of functional element, with a unified architecture for transcription initiation. The context of interacting regulatory elements and the surrounding sequences determine local transcriptional output as well as the enhancer and promoter activities of individual elements. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 06/2015; 31(8). DOI:10.1016/j.tig.2015.05.007
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    ABSTRACT: Adaptation to spatially varying environments has been studied for decades, but advances in sequencing technology are now enabling researchers to investigate the landscape of genetic variation underlying this adaptation genome wide. In this review we highlight some of the decades-long research on local adaptation in Drosophila melanogaster from well-studied clines in North America and Australia. We explore the evidence for parallel adaptation and identify commonalities in the genes responding to clinal selection across continents as well as discussing instances where patterns differ among clines. We also investigate recent studies utilizing whole-genome data to identify clines in D. melanogaster and several other systems. Although connecting segregating genomic variation to variation in phenotypes and fitness remains challenging, clinal genomics is poised to increase our understanding of local adaptation and the selective pressures that drive the extensive phenotypic diversity observed in nature. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 06/2015; 31(8). DOI:10.1016/j.tig.2015.05.006
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    ABSTRACT: The related yeasts Saccharomyces cerevisiae and Candida albicans have similar genomes but very different lifestyles. These fungi have modified transcriptional and post-translational regulatory processes to adapt their similar genomes to the distinct biological requirements of the two yeasts. We review recent findings comparing the differences between these species, highlighting how they have achieved specialized metabolic capacities tailored to their lifestyles despite sharing similar genomes. Studying this transcriptional and post-transcriptional rewiring may improve our ability to interpret phenotype from genotype. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 06/2015; 31(8). DOI:10.1016/j.tig.2015.05.002
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    ABSTRACT: Transcription factors are important determinants of lineage specification during hematopoiesis. They favor recruitment of cofactors involved in epigenetic regulation, thereby defining patterns of gene expression in a development- and lineage-specific manner. Additionally, transcription factors can facilitate transcription preinitiation complex (PIC) formation and assembly on chromatin. Interestingly, a few lineage-specific transcription factors, including IKAROS, also regulate transcription elongation. IKAROS is a tumor suppressor frequently inactivated in leukemia and associated with a poor prognosis. It forms a complex with the nucleosome remodeling and deacetylase (NuRD) complex and the positive transcription elongation factor b (P-TEFb), which is required for productive transcription elongation. It has also been reported that IKAROS interacts with factors involved in transcription termination. Here we review these and other recent findings that establish IKAROS as the first transcription factor found to act as a multifunctional regulator of the transcription cycle in hematopoietic cells. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Genetics 06/2015; 31(9). DOI:10.1016/j.tig.2015.05.003