Trends in Genetics (TRENDS GENET )

Publisher: Elsevier

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.

  • Impact factor
    9.77
    Show impact factor history
     
    Impact factor
  • 5-year impact
    9.33
  • Cited half-life
    8.30
  • Immediacy index
    2.10
  • Eigenfactor
    0.03
  • Article influence
    4.75
  • 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

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Voluntary deposit by author of pre-print allowed on Institutions open scholarly website and pre-print servers
    • Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository
    • Deposit due to Funding Body, Institutional and Governmental mandate only allowed where separate agreement between repository and publisher exists
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PMC after 12 months
    • Authors who are required to deposit in subject repositories may also use Sponsorship Option
    • Pre-print can not be deposited for The Lancet
  • Classification
    ​ green

Publications in this journal

  • [show abstract] [hide abstract]
    ABSTRACT: Genome-wide association studies (GWAS) have identified more than 8900 genetic variants, mainly single-nucleotide polymorphisms (SNPs), associated with hundreds of human traits and diseases, which define risk-associated loci. Variants that map to coding regions can affect protein sequence, translation rate, and alternative splicing, all of which influence protein function. However, the vast majority of sequence variants map to non-coding intergenic and intronic regions, and it has been much more challenging to assess the functional nature of these variants. Recent work annotating the non-coding regions of the genome has contributed to post-GWAS studies by facilitating the identification of the functional targets of risk-associated loci. Many non-coding genetic variants within risk-associated loci alter gene expression by modulating the activity of cis-regulatory elements. We review here these recent findings, discuss their implication for the post-GWAS era, and relate their importance to the interpretation of disease-associated mutations identified through whole-genome sequencing.
    Trends in Genetics 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: The availability of sequenced genomes from multiple related organisms allows the detection and localization of functional genomic elements based on the idea that such elements evolve more slowly than neutral sequences. Although such comparative genomics methods have proven useful in discovering functional elements and ascertaining levels of functional constraint in the genome as a whole, here we outline limitations intrinsic to this approach that cannot be overcome by sequencing more species. We argue that it is essential to supplement comparative genomics with ultra-deep sampling of populations from closely related species to enable substantially more powerful genomic scans for functional elements. The convergence of sequencing technology and population genetics theory has made such projects feasible and has exciting implications for functional genomics.
    Trends in Genetics 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Sport fishermen keep tension on their lines to prevent hooked fish from releasing. A molecular version of this angler's trick, operating at kinetochores, ensures accuracy during mitosis: the mitotic spindle attaches randomly to chromosomes and then correctly bioriented attachments are stabilized due to the tension exerted on them by opposing microtubules. Incorrect attachments, which lack tension, are unstable and release quickly, allowing another chance for biorientation. Stabilization of molecular interactions by tension also occurs in other physiological contexts, such as cell adhesion, motility, hemostasis, and tissue morphogenesis. Here, we review models for the stabilization of kinetochore attachments with an eye toward emerging models for other force-activated systems. Although attention in the mitosis field has focused mainly on one kinase-based mechanism, multiple mechanisms may act together to stabilize properly bioriented kinetochores and some principles governing other tension-sensitive systems may also apply to kinetochores.
    Trends in Genetics 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: High-throughput sequencing, large-scale data generation projects, and web-based cloud computing are changing how computational biology is performed, who performs it, and what biological insights it can deliver. I review here the latest developments in available data, methods, and software, focusing on the modeling and analysis of the gene regulatory interactions in cells. Three key findings are: (i) although sophisticated computational resources are increasingly available to bench biologists, tailored ongoing education is necessary to avoid the erroneous use of these resources. (ii) Current models of the regulation of gene expression are far too simplistic and need updating. (iii) Integrative computational analysis of large-scale datasets is becoming a fundamental component of molecular biology. I discuss current and near-term opportunities and challenges related to these three points.
    Trends in Genetics 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Genome-wide association studies (GWAS) have provided valuable insights into the genetic basis of complex traits, discovering >6000 variants associated with >500 quantitative traits and common complex diseases in humans. The associations identified so far represent only a fraction of those that influence phenotype, because there are likely to be many variants across the entire frequency spectrum, each of which influences multiple traits, with only a small average contribution to the phenotypic variance. This presents a considerable challenge to further dissection of the remaining unexplained genetic variance within populations, which limits our ability to predict disease risk, identify new drug targets, improve and maintain food sources, and understand natural diversity. This challenge will be met within the current framework through larger sample size, better phenotyping, including recording of nongenetic risk factors, focused study designs, and an integration of multiple sources of phenotypic and genetic information. The current evidence supports the application of quantitative genetic approaches, and we argue that one should retain simpler theories until simplicity can be traded for greater explanatory power.
    Trends in Genetics 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Evolutionary conservation is widely used as an indicator of the functional significance of newly discovered genes. Although the simple search for homology at the nucleotide or amino acid sequence level has proven to be valuable for protein-coding genes, these criteria are too narrow to describe fully the selection process for long noncoding RNAs (lncRNAs). LncRNA conservation includes four dimensions: the sequence, structure, function, and expression from syntenic loci. Two recently described knockout mouse models for the lincRNAs metastasis associated lung adenocarcinoma transcript 1 (Malat1) and HOX antisense intergenic RNA (Hotair) highlight the multifaceted levels of conservation.
    Trends in Genetics 03/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: To combat potentially deadly viral infections, prokaryotic microbes enlist small RNA-based adaptive immune systems (CRISPR-Cas systems) that protect through sequence-specific recognition and targeted destruction of viral nucleic acids (either DNA or RNA depending on the system). Here, we summarize rapid progress made in redirecting the nuclease activities of these microbial immune systems to bind and cleave DNA or RNA targets of choice, by reprogramming the small guide RNAs of the various CRISPR-Cas complexes. These studies have demonstrated the potential of Type II CRISPR-Cas systems both as efficient and versatile genome-editing tools and as potent and specific regulators of gene expression in a broad range of cell types (including human) and organisms. Progress is also being made in developing a Type III RNA-targeting CRISPR-Cas system as a novel gene knockdown platform to investigate gene function and modulate gene expression for metabolic engineering in microbes.
    Trends in Genetics 02/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: Heterochromatin protein 1 (HP1a in Drosophila) is a conserved eukaryotic chromosomal protein that is prominently associated with pericentric heterochromatin and mediates the concomitant gene silencing. Mechanistic studies implicate HP1 family proteins as 'hub proteins,' able to interact with a variety of chromosomal proteins through the chromo-shadow domain (CSD), as well as to recognize key histone modification sites [primarily histone H3 di/trimethyl Lys9 (H3K9me2/3)] through the chromodomain (CD). Consequently, HP1 has many important roles in chromatin architecture and impacts both gene expression and gene silencing, utilizing a variety of mechanisms. Clearly, HP1 function is altered by context, and potentially by post-translational modifications (PTMs). Here, we report on recent ideas as to how this versatile protein accomplishes its diverse functions.
    Trends in Genetics 02/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: DNA damage checkpoints are important tumor-suppressor mechanisms that halt cell cycle progression to allow time for DNA repair, or induce senescence and apoptosis to remove damaged cells permanently. Non-cell-autonomous DNA damage responses activate the innate immune system in multiple metazoan species. These responses not only enable clearance of damaged cells and contribute to tissue remodeling and regeneration but can also result in chronic inflammation and tissue damage. Germline DNA damage-induced systemic stress resistance (GDISR) is mediated by an ancestral innate immune response and results in organismal adjustments to the presence of damaged cells. We discuss GDISR as an organismal DNA damage checkpoint mechanism through which elevated somatic endurance can extend reproductive lifespan when germ cells require extended time for restoring genome stability.
    Trends in Genetics 01/2014;
  • [show abstract] [hide abstract]
    ABSTRACT: There are over 28 million CpG sites in the human genome. Assessing the methylation status of each of these sites will be required to understand fully the role of DNA methylation in health and disease. Genome-wide analysis, using arrays and high-throughput sequencing, has enabled assessment of large fractions of the methylome, but each protocol comes with unique advantages and disadvantages. Notably, except for whole-genome bisulfite sequencing, most commonly used genome-wide methods detect <5% of all CpG sites. Here, we discuss approaches for methylome studies and compare genome coverage of promoters, genes, and intergenic regions, and capacity to quantitate individual CpG methylation states. Finally, we examine the extent of published cancer methylomes that have been generated using genome-wide approaches.
    Trends in Genetics 12/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: Centromeres are essential for chromosome inheritance and genome stability. Centromeric proteins, including the centromeric histone centromere protein A (CENP-A), define the site of centromeric chromatin and kinetochore assembly. In many organisms, centromeres are located in or near regions of repetitive DNA. However, some atypical centromeres spontaneously form on unique sequences. These neocentromeres, or new centromeres, were first identified in humans, but have since been described in other organisms. Neocentromeres are functionally and structurally similar to endogenous centromeres, but lack the added complication of underlying repetitive sequences. Here, we discuss recent studies in chicken and fungal systems where genomic engineering can promote neocentromere formation. These studies reveal key genomic and epigenetic factors that support de novo centromere formation in eukaryotes.
    Trends in Genetics 12/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: Genotype-phenotype relations are usually inferred from a deterministic point of view. For example, quantitative trait loci (QTL), which describe regions of the genome associated with a particular phenotype, are based on a mean trait difference between genotype categories. However, living systems comprise huge numbers of cells (the 'particles' of biology). Each cell can exhibit substantial phenotypic individuality, which can have dramatic consequences at the organismal level. Now, with technology capable of interrogating individual cells, it is time to consider how genotypes shape the probability laws of single cell traits. The possibility of mapping single cell probabilistic trait loci (PTL), which link genomic regions to probabilities of cellular traits, is a promising step in this direction. This approach requires thinking about phenotypes in probabilistic terms, a concept that statistical physicists have been applying to particles for a century. Here, I describe PTL and discuss their potential to enlarge our understanding of genotype-phenotype relations.
    Trends in Genetics 12/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: Polarized transport of the hormone auxin plays crucial roles in many processes in plant development. A self-organizing pattern of auxin transport - canalization - is thought to be responsible for vascular patterning and shoot branching regulation in flowering plants. Mathematical modeling has demonstrated that membrane localization of PIN-FORMED (PIN)-family auxin efflux carriers in proportion to net auxin flux can plausibly explain canalization and possibly other auxin transport phenomena. Other plausible models have also been proposed, and there has recently been much interest in producing a unified model of all auxin transport phenomena. However, it is our opinion that lacunae in our understanding of auxin transport biology are now limiting progress in developing the next generation of models. Here we examine several key areas where significant experimental advances are necessary to address both biological and theoretical aspects of auxin transport, including the possibility of a unified transport model.
    Trends in Genetics 11/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: Elucidation of the genetic pathways that control red blood cell development has been a central goal of erythropoiesis research over the past decade. Notably, data from several recent studies have provided new insights into the regulation of erythroid gene transcription. Transcription profiling demonstrates that erythropoiesis is mainly controlled by a small group of lineage-restricted transcription factors [Gata binding protein 1 (Gata1), T cell acute lymphocytic leukemia 1 protein (Tal1), and Erythroid Kruppel-like factor (EKLF; henceforth referred to as Klf1)]. Binding-site mapping using ChIP-Seq indicates that most DNA-bound Gata1 and Tal1 proteins are contained within higher order complexes (Ldb1 complexes) that include the nuclear adapters Ldb1 and Lmo2. Ldb1 complexes regulate Klf1, and Ldb1 complex-binding sites frequently colocalize with Klf1 at erythroid genes and cis-regulatory elements, indicating strong functional synergy between Gata1, Tal1, and Klf1. Together with new data demonstrating that Ldb1 can mediate long-range promoter-enhancer interactions, these findings provide a foundation for the first comprehensive models of the global regulation of erythroid gene transcription.
    Trends in Genetics 11/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: Most severe forms of intellectual disability (ID) have specific genetic causes. Numerous X chromosome gene defects and disease-causing copy-number variants have been linked to ID and related disorders, and recent studies have revealed that sporadic cases are often due to dominant de novo mutations with low recurrence risk. For autosomal recessive ID (ARID) the recurrence risk is high and, in populations with frequent parental consanguinity, ARID is the most common form of ID. Even so, its elucidation has lagged behind. Here we review recent progress in this field, show that ARID is not rare even in outbred Western populations, and discuss the prospects for improving its diagnosis and prevention.
    Trends in Genetics 10/2013;
  • [show abstract] [hide abstract]
    ABSTRACT: Hemophilia B is a classic, monogenic blood clotting disease caused by mutations in the coagulation factor IX (F9) locus. Although interpreting mutations within the gene itself has been relatively straightforward, ascribing molecular mechanisms to the complete suite of mutations within the promoter region has proven somewhat difficult and has only recently been achieved. These mutations, which are clustered at discrete transcription factor binding sites, dynamically alter the developmental expression of F9 in different ways. They illustrate how single-nucleotide mutations in cis-regulatory regions can have drastic ramifications for the control of gene expression and in some instances be causative of disease. Here we present the human F9 promoter as a model example for which saturation mutation mapping has revealed the mechanisms of its regulation. Moreover, we suggest that the growing number of genome-wide studies of transcription factor activity will accelerate both the discovery and understanding of regulatory polymorphisms and mutations.
    Trends in Genetics 10/2013;

Related Journals