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  • Articles  (269)
  • Oxford University Press  (269)
  • 2010-2014  (135)
  • 2005-2009  (61)
  • 2000-2004  (27)
  • 1990-1994  (30)
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  • Biology  (257)
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  • Articles  (269)
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  • 1
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    The expressive power of first-order topological languages (2013)
    Oxford University Press
    Details
    Publication Date: 2013-09-26
    Description: We consider the expressive power of the first-order structure 〈, C 〉 where is either of two of different domains of extended regions in Euclidean space, and C(x,y) is the topological relation ‘Region x is in contact with region y .’ We prove two main theorems: Let $$\mathcal{P}$$ [Q] be the domain of bounded, non-empty, rational polyhedra in two- or three-dimensional Euclidean space. A relation over $$\mathcal{P}$$ [Q] is definable in the structure 〈 $$\mathcal{P}$$ [Q], C 〉 if and only if is arithmetic and invariant under rational PL-homeomorphisms of the space to itself. We also extend this result to a number of other domains, including the domain of all polyhedra and the domain of semi-algebraic regions. Let $$\mathcal{R}$$ be the space of bounded, non-empty, closed regular regions in n -dimensional Euclidean space. Any analytical relation over lower dimensional (i.e. empty interior) compact point sets that is invariant under homeomorphism is implicitly definable in the structure 〈 $$\mathcal{R}$$ , C 〉.
    Print ISSN: 0955-792X
    Electronic ISSN: 1465-363X
    Topics: Computer Science , Mathematics
    Published by Oxford University Press
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  • 2
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    Study of PcaV from Streptomyces coelicolor yields new insights into ligand-responsive MarR family transcription factors (2013)
    Oxford University Press
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    Publication Date: 2013-04-02
    Description: MarR family proteins constitute a group of 〉12 000 transcriptional regulators encoded in bacterial and archaeal genomes that control gene expression in metabolism, stress responses, virulence and multi-drug resistance. There is much interest in defining the molecular mechanism by which ligand binding attenuates the DNA-binding activities of these proteins. Here, we describe how PcaV, a MarR family regulator in Streptomyces coelicolor, controls transcription of genes encoding β-ketoadipate pathway enzymes through its interaction with the pathway substrate, protocatechuate. This transcriptional repressor is the only MarR protein known to regulate this essential pathway for aromatic catabolism. In in vitro assays, protocatechuate and other phenolic compounds disrupt the PcaV–DNA complex. We show that PcaV binds protocatechuate in a 1:1 stoichiometry with the highest affinity of any MarR family member. Moreover, we report structures of PcaV in its apo form and in complex with protocatechuate. We identify an arginine residue that is critical for ligand coordination and demonstrate that it is also required for binding DNA. We propose that interaction of ligand with this arginine residue dictates conformational changes that modulate DNA binding. Our results provide new insights into the molecular mechanism by which ligands attenuate DNA binding in this large family of transcription factors.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 3
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    Lack of CCM1 induces hypersprouting and impairs response to flow (2014)
    Oxford University Press
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    Publication Date: 2014-11-07
    Description: Cerebral cavernous malformation (CCM) is a disease of vascular malformations known to be caused by mutations in one of three genes: CCM1 , CCM2 or CCM3 . Despite several studies, the mechanism of CCM lesion onset remains unclear. Using a Ccm1 knockout mouse model, we studied the morphogenesis of early lesion formation in the retina in order to provide insight into potential mechanisms. We demonstrate that lesions develop in a stereotypic location and pattern, preceded by endothelial hypersprouting as confirmed in a zebrafish model of disease. The vascular defects seen with loss of Ccm1 suggest a defect in endothelial flow response. Taken together, these results suggest new mechanisms of early CCM disease pathogenesis and provide a framework for further study.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 4
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    The Comparative Toxicogenomics Database: update 2013 (2012)
    Oxford University Press
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    Publication Date: 2012-12-20
    Description: The Comparative Toxicogenomics Database (CTD; http://ctdbase.org/ ) provides information about interactions between environmental chemicals and gene products and their relationships to diseases. Chemical–gene, chemical–disease and gene–disease interactions manually curated from the literature are integrated to generate expanded networks and predict many novel associations between different data types. CTD now contains over 15 million toxicogenomic relationships. To navigate this sea of data, we added several new features, including DiseaseComps (which finds comparable diseases that share toxicogenomic profiles), statistical scoring for inferred gene–disease and pathway–chemical relationships, filtering options for several tools to refine user analysis and our new Gene Set Enricher (which provides biological annotations that are enriched for gene sets). To improve data visualization, we added a Cytoscape Web view to our ChemComps feature, included color-coded interactions and created a ‘slim list’ for our MEDIC disease vocabulary (allowing diseases to be grouped for meta-analysis, visualization and better data management). CTD continues to promote interoperability with external databases by providing content and cross-links to their sites. Together, this wealth of expanded chemical–gene–disease data, combined with novel ways to analyze and view content, continues to help users generate testable hypotheses about the molecular mechanisms of environmental diseases.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 5
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    STAR: ultrafast universal RNA-seq aligner (2012)
    Oxford University Press
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    Publication Date: 2012-12-21
    Description: Motivation: Accurate alignment of high-throughput RNA-seq data is a challenging and yet unsolved problem because of the non-contiguous transcript structure, relatively short read lengths and constantly increasing throughput of the sequencing technologies. Currently available RNA-seq aligners suffer from high mapping error rates, low mapping speed, read length limitation and mapping biases. Results: To align our large (〉80 billon reads) ENCODE Transcriptome RNA-seq dataset, we developed the Spliced Transcripts Alignment to a Reference (STAR) software based on a previously undescribed RNA-seq alignment algorithm that uses sequential maximum mappable seed search in uncompressed suffix arrays followed by seed clustering and stitching procedure. STAR outperforms other aligners by a factor of 〉50 in mapping speed, aligning to the human genome 550 million 2 x 76 bp paired-end reads per hour on a modest 12-core server, while at the same time improving alignment sensitivity and precision. In addition to unbiased de novo detection of canonical junctions, STAR can discover non-canonical splices and chimeric (fusion) transcripts, and is also capable of mapping full-length RNA sequences. Using Roche 454 sequencing of reverse transcription polymerase chain reaction amplicons, we experimentally validated 1960 novel intergenic splice junctions with an 80–90% success rate, corroborating the high precision of the STAR mapping strategy. Availability and implementation: STAR is implemented as a standalone C++ code. STAR is free open source software distributed under GPLv3 license and can be downloaded from http://code.google.com/p/rna-star/ . Contact: dobin@cshl.edu .
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 6
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    Mutations in FKBP10, which result in Bruck syndrome and recessive forms of osteogenesis imperfecta, inhibit the hydroxylation of telopeptide lysines in bone collagen (2012)
    Oxford University Press
    Details
    Publication Date: 2012-12-15
    Description: Although biallelic mutations in non-collagen genes account for 〈10% of individuals with osteogenesis imperfecta, the characterization of these genes has identified new pathways and potential interventions that could benefit even those with mutations in type I collagen genes. We identified mutations in FKBP10 , which encodes the 65 kDa prolyl cis–trans isomerase, FKBP65, in 38 members of 21 families with OI. These include 10 families from the Samoan Islands who share a founder mutation. Of the mutations, three are missense; the remainder either introduce premature termination codons or create frameshifts both of which result in mRNA instability. In four families missense mutations result in loss of most of the protein. The clinical effects of these mutations are short stature, a high incidence of joint contractures at birth and progressive scoliosis and fractures, but there is remarkable variability in phenotype even within families. The loss of the activity of FKBP65 has several effects: type I procollagen secretion is slightly delayed, the stabilization of the intact trimer is incomplete and there is diminished hydroxylation of the telopeptide lysyl residues involved in intermolecular cross-link formation in bone. The phenotype overlaps with that seen with mutations in PLOD2 (Bruck syndrome II), which encodes LH2, the enzyme that hydroxylates the telopeptide lysyl residues. These findings define a set of genes, FKBP10 , PLOD2 and SERPINH1 , that act during procollagen maturation to contribute to molecular stability and post-translational modification of type I procollagen, without which bone mass and quality are abnormal and fractures and contractures result.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 7
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    Characterization of behavioral and neuromuscular junction phenotypes in a novel allelic series of SMA mouse models (2012)
    Oxford University Press
    Details
    Publication Date: 2012-09-28
    Description: A number of mouse models for spinal muscular atrophy (SMA) have been genetically engineered to recapitulate the severity of human SMA by using a targeted null mutation at the mouse Smn1 locus coupled with the transgenic addition of varying copy numbers of human SMN2 genes. Although this approach has been useful in modeling severe SMA and very mild SMA, a mouse model of the intermediate form of the disease would provide an additional research tool amenable for drug discovery. In addition, many of the previously engineered SMA strains are multi-allelic by design, containing a combination of transgenes and targeted mutations in the homozygous state, making further genetic manipulation difficult. A new genetic engineering approach was developed whereby variable numbers of SMN2 sequences were incorporated directly into the murine Smn1 locus. Using combinations of these alleles, we generated an allelic series of SMA mouse strains harboring no, one, two, three, four, five, six or eight copies of SMN2. We report here the characterization of SMA mutants in this series that displayed a range in disease severity from embryonic lethal to viable with mild neuromuscular deficits.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 8
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    JETTA: junction and exon toolkits for transcriptome analysis (2012)
    Oxford University Press
    Details
    Publication Date: 2012-04-28
    Description: : High-throughput genome-wide studies of alternatively spliced mRNA transcripts have become increasingly important in clinical research. Consequently, easy-to-use software tools are required to process data from these studies, for example, using exon and junction arrays. Here, we introduce JETTA, an integrated software package for the calculation of gene expression indices as well as the identification and visualization of alternative splicing events. We demonstrate the software using data of human liver and muscle samples hybridized on an exon–junction array. Availability: JETTA and its demonstrations are freely available at http://igenomed.stanford.edu/~junhee/JETTA/index.html Contacts: wxiao1@partners.org
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
    Published by Oxford University Press
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  • 9
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    Observations of discards in the Scottish mixed demersal trawl fishery (2011)
    Oxford University Press
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    Publication Date: 2011-11-24
    Description: Fernandes, P. G., Coull, K., Davis, C., Clark, P., Catarino, R., Bailey, N., Fryer, R., and Pout, A. 2011. Observations of discards in the Scottish mixed demersal trawl fishery. – ICES Journal of Marine Science, 68: 1734–1742. The Marine Laboratory in Aberdeen (now part of Marine Scotland Science) has operated a scientific observer programme in the Scottish mixed demersal trawl fishery for more than 20 years. Discards of the main demersal species (cod, haddock, whiting, and saithe) have been sampled according to a stratified design based on gear, area, and month, with quota sampling used to select vessels. The aim of the programme is to estimate the quantity (at age) of the discarded component of the catch, to contribute to estimates of total catch for these species so that assessments of each stock can be made. Trends of discards from this observer programme from 1987 to 2009 are reported. Notable features include the sudden practice of discarding marketable cod in 2007. This was due to a number of factors including, paradoxically, improvements in compliance measures which meant that fish could no longer be landed illegally. Methods for raising the sampled discards to the level of the fleet are also explored and discussed in relation to changes in discarding patterns. These are particularly relevant at a time when, in northern Europe at least, there is a move towards standardizing methods for estimating total quantities of discards.
    Print ISSN: 1054-3139
    Electronic ISSN: 1095-9289
    Topics: Biology , Geosciences , Physics
    Published by Oxford University Press
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  • 10
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    Letter to the Glycoforum Transforming Glycoscience: An Australian Perspective (2013)
    Oxford University Press
    Details
    Publication Date: 2013-12-07
    Print ISSN: 0959-6658
    Electronic ISSN: 1460-2423
    Topics: Biology , Medicine
    Published by Oxford University Press
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