Honaïn

Sur la côte d’Oranie, à 52 kilomètres de la frontière marocaine, se creuse une baie à laquelle des hauteurs escarpées donnent des allures de fjord. Une plage en occupe le fond et, derrière la plage, l’enceinte d’une ville se dessine, escaladant les pentes de la montagne. Cette ville, ou plutôt cette coquille de ville vidée de son contenu, c’est Honaïn, dont le nom figure à maintes reprises chez les chroniqueurs et les géographes du Moyen Âge. Nul centre antique ne paraît l’avoir précédée, à m..

Honaïn

Sur la côte d’Oranie, à 52 kilomètres de la frontière marocaine, se creuse une baie à laquelle des hauteurs escarpées donnent des allures de fjord. Une plage en occupe le fond et, derrière la plage, l’enceinte d’une ville se dessine, escaladant les pentes de la montagne. Cette ville, ou plutôt cette coquille de ville vidée de son contenu, c’est Honaïn, dont le nom figure à maintes reprises chez les chroniqueurs et les géographes du Moyen Âge. Nul centre antique ne paraît l’avoir précédée, à m..

Honaïn

Sur la côte d’Oranie, à 52 kilomètres de la frontière marocaine, se creuse une baie à laquelle des hauteurs escarpées donnent des allures de fjord. Une plage en occupe le fond et, derrière la plage, l’enceinte d’une ville se dessine, escaladant les pentes de la montagne. Cette ville, ou plutôt cette coquille de ville vidée de son contenu, c’est Honaïn, dont le nom figure à maintes reprises chez les chroniqueurs et les géographes du Moyen Âge. Nul centre antique ne paraît l’avoir précédée, à m..

A whole-genome assembly of the domestic cow, Bos taurus

Background: The genome of the domestic cow, Bos taurus, was sequenced using a mixture of hierarchical and whole-genome shotgun sequencing methods. Results: We have assembled the 35 million sequence reads and applied a variety of assembly improvement techniques, creating an assembly of 2.86 billion base pairs that has multiple improvements over previous assemblies: it is more complete, covering more of the genome; thousands of gaps have been closed; many erroneous inversions, deletions, and translocations have been corrected; and thousands of single-nucleotide errors have been corrected. Our evaluation using independent metrics demonstrates that the resulting assembly is substantially more accurate and complete than alternative versions. Conclusions: By using independent mapping data and conserved synteny between the cow and human genomes, we were able to construct an assembly with excellent large-scale contiguity in which a large majority (approximately 91%) of the genome has been placed onto the 30 B. taurus chromosomes. We constructed a new cow-human synteny map that expands upon previous maps. We also identified for the first time a portion of the B. taurus Y chromosome. © 2009 Zimin et al.; licensee BioMed Central Ltd

ccTSA: A Coverage-Centric Threaded Sequence Assembler

De novo sequencing, a process to find the whole genome or the regions of a species without references, requires much higher computational power compared to mapped sequencing with references. The advent and continuous evolution of next-generation sequencing technologies further stress the demands of high-throughput processing of myriads of short DNA fragments. Recently announced sequence assemblers, such as Velvet, SOAPdenovo, and ABySS, all exploit parallelism to meet these computational demands since contemporary computer systems primarily rely on scaling the number of computing cores to improve performance. However, most of them are not tailored to exploit the full potential of these systems, leading to suboptimal performance. In this paper, we present ccTSA, a parallel sequence assembler that utilizes coverage to prune k-mers, find preferred edges, and resolve conflicts in preferred edges between k-mers. We minimize computation dependencies between threads to effectively parallelize k-mer processing. We also judiciously allocate and reuse memory space in order to lower memory usage and further improve sequencing speed. The results of ccTSA are compelling such that it runs several times faster than other assemblers while providing comparable quality values such as N50

Efficient counting of k-mers in DNA sequences using a bloom filter

<p>Abstract</p> <p>Background</p> <p>Counting <it>k</it>-mers (substrings of length <it>k </it>in DNA sequence data) is an essential component of many methods in bioinformatics, including for genome and transcriptome assembly, for metagenomic sequencing, and for error correction of sequence reads. Although simple in principle, counting <it>k</it>-mers in large modern sequence data sets can easily overwhelm the memory capacity of standard computers. In current data sets, a large fraction-often more than 50%-of the storage capacity may be spent on storing <it>k</it>-mers that contain sequencing errors and which are typically observed only a single time in the data. These singleton <it>k</it>-mers are uninformative for many algorithms without some kind of error correction.</p> <p>Results</p> <p>We present a new method that identifies all the <it>k</it>-mers that occur more than once in a DNA sequence data set. Our method does this using a Bloom filter, a probabilistic data structure that stores all the observed <it>k</it>-mers implicitly in memory with greatly reduced memory requirements. We then make a second sweep through the data to provide exact counts of all nonunique <it>k</it>-mers. For example data sets, we report up to 50% savings in memory usage compared to current software, with modest costs in computational speed. This approach may reduce memory requirements for any algorithm that starts by counting <it>k</it>-mers in sequence data with errors.</p> <p>Conclusions</p> <p>A reference implementation for this methodology, BFCounter, is written in C++ and is GPL licensed. It is available for free download at <url>http://pritch.bsd.uchicago.edu/bfcounter.html</url></p

Impacts of climate change on plant diseases – opinions and trends

There has been a remarkable scientific output on the topic of how climate change is likely to affect plant diseases in the coming decades. This review addresses the need for review of this burgeoning literature by summarizing opinions of previous reviews and trends in recent studies on the impacts of climate change on plant health. Sudden Oak Death is used as an introductory case study: Californian forests could become even more susceptible to this emerging plant disease, if spring precipitations will be accompanied by warmer temperatures, although climate shifts may also affect the current synchronicity between host cambium activity and pathogen colonization rate. A summary of observed and predicted climate changes, as well as of direct effects of climate change on pathosystems, is provided. Prediction and management of climate change effects on plant health are complicated by indirect effects and the interactions with global change drivers. Uncertainty in models of plant disease development under climate change calls for a diversity of management strategies, from more participatory approaches to interdisciplinary science. Involvement of stakeholders and scientists from outside plant pathology shows the importance of trade-offs, for example in the land-sharing vs. sparing debate. Further research is needed on climate change and plant health in mountain, boreal, Mediterranean and tropical regions, with multiple climate change factors and scenarios (including our responses to it, e.g. the assisted migration of plants), in relation to endophytes, viruses and mycorrhiza, using long-term and large-scale datasets and considering various plant disease control methods

Chronic T cell receptor stimulation unmasks NK receptor signaling in peripheral T cell lymphomas via epigenetic reprogramming.

Peripheral T cell lymphomas (PTCLs) represent a significant unmet medical need with dismal clinical outcomes. The T cell receptor (TCR) is emerging as a key driver of T lymphocyte transformation. However, the role of chronic TCR activation in lymphomagenesis and in lymphoma cell survival is still poorly understood. Using a mouse model, we report that chronic TCR stimulation drove T cell lymphomagenesis, whereas TCR signaling did not contribute to PTCL survival. The combination of kinome, transcriptome, and epigenome analyses of mouse PTCLs revealed a NK cell-like reprogramming of PTCL cells with expression of NK receptors (NKRs) and downstream signaling molecules such as Tyrobp and SYK. Activating NKRs were functional in PTCLs and dependent on SYK activity. In vivo blockade of NKR signaling prolonged mouse survival, demonstrating the addiction of PTCLs to NKRs and downstream SYK/mTOR activity for their survival. We studied a large collection of human primary samples and identified several PTCLs recapitulating the phenotype described in this model by their expression of SYK and the NKR, suggesting a similar mechanism of lymphomagenesis and establishing a rationale for clinical studies targeting such molecules