Nature (NATURE )

Publisher: Nature Publishing Group

Description

Publishes papers from any area of science with great potential impact.

  • Impact factor
    38.60
    Show impact factor history
     
    Impact factor
  • 5-year impact
    38.16
  • Cited half-life
    9.60
  • Immediacy index
    9.24
  • Eigenfactor
    1.58
  • Article influence
    20.84
  • Website
    Nature website
  • Other titles
    Nature, International weekly journal of science
  • ISSN
    0028-0836
  • OCLC
    1586310
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Published source must be acknowledged and DOI cited
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • On author's personal website and institutional repository
    • If funding agency rules apply, authors may post authors version to their relevant funding body's archive, 6 months after publication
  • Classification
    ​ yellow

Publications in this journal

  • Piero Carninci
    Nature 11/2014; 515(7527):346-7.
  • Philip Campbell
    Nature 11/2014; 515(7527):453-4.
  • Benjamin D Pope, Tyrone Ryba, Vishnu Dileep, Feng Yue, Weisheng Wu, Olgert Denas, Daniel L Vera, Yanli Wang, R Scott Hansen, Theresa K Canfield, [......], Yong Cheng, Günhan Gülsoy, Jonathan H Dennis, Michael P Snyder, John A Stamatoyannopoulos, James Taylor, Ross C Hardison, Tamer Kahveci, Bing Ren, David M Gilbert
    [Show abstract] [Hide abstract]
    ABSTRACT: Eukaryotic chromosomes replicate in a temporal order known as the replication-timing program. In mammals, replication timing is cell-type-specific with at least half the genome switching replication timing during development, primarily in units of 400-800 kilobases ('replication domains'), whose positions are preserved in different cell types, conserved between species, and appear to confine long-range effects of chromosome rearrangements. Early and late replication correlate, respectively, with open and closed three-dimensional chromatin compartments identified by high-resolution chromosome conformation capture (Hi-C), and, to a lesser extent, late replication correlates with lamina-associated domains (LADs). Recent Hi-C mapping has unveiled substructure within chromatin compartments called topologically associating domains (TADs) that are largely conserved in their positions between cell types and are similar in size to replication domains. However, TADs can be further sub-stratified into smaller domains, challenging the significance of structures at any particular scale. Moreover, attempts to reconcile TADs and LADs to replication-timing data have not revealed a common, underlying domain structure. Here we localize boundaries of replication domains to the early-replicating border of replication-timing transitions and map their positions in 18 human and 13 mouse cell types. We demonstrate that, collectively, replication domain boundaries share a near one-to-one correlation with TAD boundaries, whereas within a cell type, adjacent TADs that replicate at similar times obscure replication domain boundaries, largely accounting for the previously reported lack of alignment. Moreover, cell-type-specific replication timing of TADs partitions the genome into two large-scale sub-nuclear compartments revealing that replication-timing transitions are indistinguishable from late-replicating regions in chromatin composition and lamina association and accounting for the reduced correlation of replication timing to LADs and heterochromatin. Our results reconcile cell-type-specific sub-nuclear compartmentalization and replication timing with developmentally stable structural domains and offer a unified model for large-scale chromosome structure and function.
    Nature 11/2014; 515(7527):402-5.
  • Andrew B Stergachis, Shane Neph, Richard Sandstrom, Eric Haugen, Alex P Reynolds, Miaohua Zhang, Rachel Byron, Theresa Canfield, Sandra Stelhing-Sun, Kristen Lee, [......], Audra K Johnson, Peter J Sabo, Matthew S Wilken, Thomas A Reh, Piper M Treuting, Rajinder Kaul, Mark Groudine, M A Bender, Elhanan Borenstein, John A Stamatoyannopoulos
    [Show abstract] [Hide abstract]
    ABSTRACT: The basic body plan and major physiological axes have been highly conserved during mammalian evolution, yet only a small fraction of the human genome sequence appears to be subject to evolutionary constraint. To quantify cis- versus trans-acting contributions to mammalian regulatory evolution, we performed genomic DNase I footprinting of the mouse genome across 25 cell and tissue types, collectively defining ∼8.6 million transcription factor (TF) occupancy sites at nucleotide resolution. Here we show that mouse TF footprints conjointly encode a regulatory lexicon that is ∼95% similar with that derived from human TF footprints. However, only ∼20% of mouse TF footprints have human orthologues. Despite substantial turnover of the cis-regulatory landscape, nearly half of all pairwise regulatory interactions connecting mouse TF genes have been maintained in orthologous human cell types through evolutionary innovation of TF recognition sequences. Furthermore, the higher-level organization of mouse TF-to-TF connections into cellular network architectures is nearly identical with human. Our results indicate that evolutionary selection on mammalian gene regulation is targeted chiefly at the level of trans-regulatory circuitry, enabling and potentiating cis-regulatory plasticity.
    Nature 11/2014; 515(7527):365-70.
  • Elizabeth Gibney
    Nature 11/2014; 515(7527):319-20.
  • Erin Biba
    Nature 11/2014; 515(7527):S124-5.
  • Josh M Gray, Steve Frolking, Eric A Kort, Deepak K Ray, Christopher J Kucharik, Navin Ramankutty, Mark A Friedl
    [Show abstract] [Hide abstract]
    ABSTRACT: Ground- and aircraft-based measurements show that the seasonal amplitude of Northern Hemisphere atmospheric carbon dioxide (CO2) concentrations has increased by as much as 50 per cent over the past 50 years. This increase has been linked to changes in temperate, boreal and arctic ecosystem properties and processes such as enhanced photosynthesis, increased heterotrophic respiration, and expansion of woody vegetation. However, the precise causal mechanisms behind the observed changes in atmospheric CO2 seasonality remain unclear. Here we use production statistics and a carbon accounting model to show that increases in agricultural productivity, which have been largely overlooked in previous investigations, explain as much as a quarter of the observed changes in atmospheric CO2 seasonality. Specifically, Northern Hemisphere extratropical maize, wheat, rice, and soybean production grew by 240 per cent between 1961 and 2008, thereby increasing the amount of net carbon uptake by croplands during the Northern Hemisphere growing season by 0.33 petagrams. Maize alone accounts for two-thirds of this change, owing mostly to agricultural intensification within concentrated production zones in the midwestern United States and northern China. Maize, wheat, rice, and soybeans account for about 68 per cent of extratropical dry biomass production, so it is likely that the total impact of increased agricultural production exceeds the amount quantified here.
    Nature 11/2014; 515(7527):398-401.
  • Mark Yarborough
    Nature 11/2014; 515(7527):313.
  • Tim Palmer
    Nature 11/2014; 515(7527):338-9.
  • Cassandra Willyard
    Nature 11/2014; 515(7527):S112-3.
  • Mark Zastrow
    Nature 11/2014; 515(7527):321.
  • Michael J Werner
    Nature 11/2014; 515(7527):S126.
  • Hope Klug
    Nature 11/2014; 515(7527):343.
  • Michelle Thew
    Nature 11/2014; 515(7527):343.
  • Philippe Ghosez, Jean-Marc Triscone
    Nature 11/2014; 515(7527):348-50.
  • Susan M Swetter, Alan C Geller
    Nature 11/2014; 515(7527):S117.
  • Julia Schmale, Drew Shindell, Erika von Schneidemesser, Ilan Chabay, Mark Lawrence
    Nature 11/2014; 515(7527):335-7.
  • Feng Yue, Yong Cheng, Alessandra Breschi, Jeff Vierstra, Weisheng Wu, Tyrone Ryba, Richard Sandstrom, Zhihai Ma, Carrie Davis, Benjamin D Pope, [......], Ali Mortazavi, Sherman M Weissman, John A Stamatoyannopoulos, Michael P Snyder, Roderic Guigo, Thomas R Gingeras, David M Gilbert, Ross C Hardison, Michael A Beer, Bing Ren
    [Show abstract] [Hide abstract]
    ABSTRACT: The laboratory mouse shares the majority of its protein-coding genes with humans, making it the premier model organism in biomedical research, yet the two mammals differ in significant ways. To gain greater insights into both shared and species-specific transcriptional and cellular regulatory programs in the mouse, the Mouse ENCODE Consortium has mapped transcription, DNase I hypersensitivity, transcription factor binding, chromatin modifications and replication domains throughout the mouse genome in diverse cell and tissue types. By comparing with the human genome, we not only confirm substantial conservation in the newly annotated potential functional sequences, but also find a large degree of divergence of sequences involved in transcriptional regulation, chromatin state and higher order chromatin organization. Our results illuminate the wide range of evolutionary forces acting on genes and their regulatory regions, and provide a general resource for research into mammalian biology and mechanisms of human diseases.
    Nature 11/2014; 515(7527):355-64.
  • Thomas R Insel, Story Landis
    Nature 11/2014; 515(7527):344.