982 research outputs found

    Semantic browsing of digital collections

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    Visiting museums is an increasingly popular pastime. Studies have shown that visitors can draw on their museum experience, long after their visit, to learn new things in practical situations. Rather than viewing a visit as a single learning event, we are interested in ways of extending the experience to allow visitors to access online resources tailored to their interests. Museums typically have extensive archives that can be made available online, the challenge is to match these resources to the visitor’s interests and present them in a manner that facilitates exploration and engages the visitor. We propose the use of knowledge level resource descriptions to identify relevant resources and create structured presentations. A system that embodies this approach, which is in use in a UK museum, is presented and the applicability of the approach to the broader semantic web is discussed

    Evaluating the semantic web: a task-based approach

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    The increased availability of online knowledge has led to the design of several algorithms that solve a variety of tasks by harvesting the Semantic Web, i.e. by dynamically selecting and exploring a multitude of online ontologies. Our hypothesis is that the performance of such novel algorithms implicity provides an insight into the quality of the used ontologies and thus opens the way to a task-based evaluation of the Semantic Web. We have investigated this hypothesis by studying the lessons learnt about online ontologies when used to solve three tasks: ontology matching, folksonomy enrichment, and word sense disambiguation. Our analysis leads to a suit of conclusions about the status of the Semantic Web, which highlight a number of strengths and weaknesses of the semantic information available online and complement the findings of other analysis of the Semantic Web landscape

    On the emergent Semantic Web and overlooked issues

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    The emergent Semantic Web, despite being in its infancy, has already received a lotof attention from academia and industry. This resulted in an abundance of prototype systems and discussion most of which are centred around the underlying infrastructure. However, when we critically review the work done to date we realise that there is little discussion with respect to the vision of the Semantic Web. In particular, there is an observed dearth of discussion on how to deliver knowledge sharing in an environment such as the Semantic Web in effective and efficient manners. There are a lot of overlooked issues, associated with agents and trust to hidden assumptions made with respect to knowledge representation and robust reasoning in a distributed environment. These issues could potentially hinder further development if not considered at the early stages of designing Semantic Web systems. In this perspectives paper, we aim to help engineers and practitioners of the Semantic Web by raising awareness of these issues

    Interplay of Mre11 Nuclease with Dna2 plus Sgs1 in Rad51-Dependent Recombinational Repair

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    The Mre11/Rad50/Xrs2 complex initiates IR repair by binding to the end of a double-strand break, resulting in 5′ to 3′ exonuclease degradation creating a single-stranded 3′ overhang competent for strand invasion into the unbroken chromosome. The nuclease(s) involved are not well understood. Mre11 encodes a nuclease, but it has 3′ to 5′, rather than 5′ to 3′ activity. Furthermore, mutations that inactivate only the nuclease activity of Mre11 but not its other repair functions, mre11-D56N and mre11-H125N, are resistant to IR. This suggests that another nuclease can catalyze 5′ to 3′ degradation. One candidate nuclease that has not been tested to date because it is encoded by an essential gene is the Dna2 helicase/nuclease. We recently reported the ability to suppress the lethality of a dna2Δ with a pif1Δ. The dna2Δ pif1Δ mutant is IR-resistant. We have determined that dna2Δ pif1Δ mre11-D56N and dna2Δ pif1Δ mre11-H125N strains are equally as sensitive to IR as mre11Δ strains, suggesting that in the absence of Dna2, Mre11 nuclease carries out repair. The dna2Δ pif1Δ mre11-D56N triple mutant is complemented by plasmids expressing Mre11, Dna2 or dna2K1080E, a mutant with defective helicase and functional nuclease, demonstrating that the nuclease of Dna2 compensates for the absence of Mre11 nuclease in IR repair, presumably in 5′ to 3′ degradation at DSB ends. We further show that sgs1Δ mre11-H125N, but not sgs1Δ, is very sensitive to IR, implicating the Sgs1 helicase in the Dna2-mediated pathway

    DNA end resection by Dna2–Sgs1–RPA and its stimulation by Top3–Rmi1 and Mre11–Rad50–Xrs2

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    The repair of DNA double-strand breaks (DSBs) by homologous recombination requires processing of broken ends. For repair to start, the DSB must first be resected to generate a 3′-single-stranded DNA (ssDNA) overhang, which becomes a substrate for the DNA strand exchange protein, Rad51 (ref. 1). Genetic studies have implicated a multitude of proteins in the process, including helicases, nucleases and topoisomerases. Here we biochemically reconstitute elements of the resection process and reveal that it requires the nuclease Dna2, the RecQ-family helicase Sgs1 and the ssDNA-binding protein replication protein-A (RPA). We establish that Dna2, Sgs1 and RPA constitute a minimal protein complex capable of DNA resection in vitro. Sgs1 helicase unwinds the DNA to produce an intermediate that is digested by Dna2, and RPA stimulates DNA unwinding by Sgs1 in a species-specific manner. Interestingly, RPA is also required both to direct Dna2 nucleolytic activity to the 5′-terminated strand of the DNA break and to inhibit 3′ to 5′ degradation by Dna2, actions that generate and protect the 3′-ssDNA overhang, respectively. In addition to this core machinery, we establish that both the topoisomerase 3 (Top3) and Rmi1 complex and the Mre11–Rad50–Xrs2 complex (MRX) have important roles as stimulatory components. Stimulation of end resection by the Top3–Rmi1 heterodimer and the MRX proteins is by complex formation with Sgs1 (refs 5, 6), which unexpectedly stimulates DNA unwinding. We suggest that Top3–Rmi1 and MRX are important for recruitment of the Sgs1–Dna2 complex to DSBs. Our experiments provide a mechanistic framework for understanding the initial steps of recombinational DNA repair in eukaryotes

    The Ecm11-Gmc2 complex promotes synaptonemal complex formation through assembly of transverse filaments in budding yeast

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    During meiosis, homologous chromosomes pair at close proximity to form the synaptonemal complex (SC). This association is mediated by transverse filament proteins that hold the axes of homologous chromosomes together along their entire length. Transverse filament proteins are highly aggregative and can form an aberrant aggregate called the polycomplex that is unassociated with chromosomes. Here, we show that the Ecm11-Gmc2 complex is a novel SC component, functioning to facilitate assembly of the yeast transverse filament protein, Zip1. Ecm11 and Gmc2 initially localize to the synapsis initiation sites, then throughout the synapsed regions of paired homologous chromosomes. The absence of either Ecm11 or Gmc2 substantially compromises the chromosomal assembly of Zip1 as well as polycomplex formation, indicating that the complex is required for extensive Zip1 polymerization. We also show that Ecm11 is SUMOylated in a Gmc2-dependent manner. Remarkably, in the unSUMOylatable ecm11 mutant, assembly of chromosomal Zip1 remained compromised while polycomplex formation became frequent. We propose that the Ecm11-Gmc2 complex facilitates the assembly of Zip1 and that SUMOylation of Ecm11 is critical for ensuring chromosomal assembly of Zip1, thus suppressing polycomplex formation

    A new energy consumption technique for mobile ad hoc networks

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    A dynamic temporary network is created through wireless mobile nodes without the need for considerable infrastructure as well as a central manager. In a mobile ad hoc network, routing protocols allow a mobile for transmission and receiving packets. In the last decade, many variants have come up for the AODV. A minimum number of hop counts are chosen for enhancing routing protocols to include additional factors that can have an impact on path selections. As the distance between each node grows, the transmission power also rises accordingly. Hence, this impacts the network’s entire performance and the most important feature is the quality of service. Most of the traditional routing protocols include energy consumption levels of the nodes and various parameters, like residual battery power, consumption of energy per packet and energy needed per transmission. A new technique is proposed in this paper to enhance the routing efficiency by making use of lion optimization algorithm after identifying all possible paths in the network. This technique not only enhances the energy efficiency of each node but also the performance metrics

    Budding yeast ATM/ATR control meiotic double-strand break (DSB) levels by down-regulating Rec114, an essential component of the DSB-machinery

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    An essential feature of meiosis is Spo11 catalysis of programmed DNA double strand breaks (DSBs). Evidence suggests that the number of DSBs generated per meiosis is genetically determined and that this ability to maintain a pre-determined DSB level, or "DSB homeostasis", might be a property of the meiotic program. Here, we present direct evidence that Rec114, an evolutionarily conserved essential component of the meiotic DSB-machinery, interacts with DSB hotspot DNA, and that Tel1 and Mec1, the budding yeast ATM and ATR, respectively, down-regulate Rec114 upon meiotic DSB formation through phosphorylation. Mimicking constitutive phosphorylation reduces the interaction between Rec114 and DSB hotspot DNA, resulting in a reduction and/or delay in DSB formation. Conversely, a non-phosphorylatable rec114 allele confers a genome-wide increase in both DSB levels and in the interaction between Rec114 and the DSB hotspot DNA. These observations strongly suggest that Tel1 and/or Mec1 phosphorylation of Rec114 following Spo11 catalysis down-regulates DSB formation by limiting the interaction between Rec114 and DSB hotspots. We also present evidence that Ndt80, a meiosis specific transcription factor, contributes to Rec114 degradation, consistent with its requirement for complete cessation of DSB formation. Loss of Rec114 foci from chromatin is associated with homolog synapsis but independent of Ndt80 or Tel1/Mec1 phosphorylation. Taken together, we present evidence for three independent ways of regulating Rec114 activity, which likely contribute to meiotic DSBs-homeostasis in maintaining genetically determined levels of breaks
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