This is an RSS newsfeed from BioMed Central It is intended to be used with an RSS reader. For more information about RSS newsfeeds from BioMed Central, visit http://www.biomedcentral.com/info/about/rss/ http://genomebiology.com/ The latest articles from Genome Biology (ISSN 1465-6906) published by BioMed Central Background: Viruses are ubiquitous and the most abundant biological entities in marine environments. Metagenomics studies are increasingly revealing the huge genetic diversity of marine viruses. In this study, we used a new approach - "phylogenetic mapping" - to obtain a comprehensive picture of the taxonomic distribution of large DNA viruses represented in the Sorcerer II Global Ocean Sampling Expedition metagenomic data set. Results: Using DNA polymerase genes as a taxonomic marker, we identified 811 homologous sequences of likely viral origins. As expected, most of these sequences corresponded to phages. Interestingly, the second largest viral group corresponded to the one containing mimivirus and three related algal viruses. We also identified several DNA polymerase homologs closely related to Asfarviridae, a viral family poorly represented among isolated viruses and until now limited to terrestrial animal hosts. Finally, our approach allowed the identification of a new combination of genes in "viral-like" sequences. Conclusions: Albeit only recently discovered, giant viruses of the Mimiviridae family appear to constitute a diverse, quantitatively important and ubiquitous component of the population of large eukaryotic DNA viruses in the sea. http://genomebiology.com/2008/9/7/R106 Adam Monier, Jean-Michel Claverie and Hiroyuki Ogata Genome Biology 2008, 9:R106 2008-07-03 doi:10.1186/gb-2008-9-7-r106 Genome Biology 1465-6906 9 R106 2008-07-03 Background: Sequencing and annotation of several mammalian genomes have revealed that segmental duplications are a common architectural feature of primate genomes; in fact, about 5% of the human genome is comprised of large blocks of interspersed segmental duplications. These segmental duplications have been implicated in genomic copy-number variation, gene novelty, and various genomic disorders. However, the molecular processes involved in the evolution and regulation of duplicated sequences remain largely unexplored. Results: In this study, the profile of about 20 histone modifications within human segmental duplications was characterized using high-resolution, genome-wide data derived from a ChIP-Seq study. The analysis demonstrated that derivative loci of segmental duplications often differ significantly from the original with respect to many histone methylations. Further investigation showed that genes are present 3x more frequently in the original than in the derivative, whereas pseudogenes exhibit the opposite trend. These asymmetries tend to increase with the age of segmental duplications. The uneven distribution of genes and pseudogenes did not, however, fully account for the asymmetry in the profile of histone modifications. Conclusions: The first systematic analysis of histone modifications between segmental duplications demonstrates that two seemingly "identical" genomic copies are distinct in their epigenomic properties. Results here suggest that local chromatin environments may be implicated in the discrimination of derived copies of segmental duplications from their originals, leading to a biased pseudogenization of the new duplicates. The data also indicate that further exploration of the interactions between histone modification and sequence degeneration is necessary in order to understand the divergence of duplicated sequences. http://genomebiology.com/2008/9/7/R105 Deyou Zheng Genome Biology 2008, 9:R105 2008-07-03 doi:10.1186/gb-2008-9-7-r105 Genome Biology 1465-6906 9 R105 2008-07-03 A report on the conference 'Systems Genomics 2008', Heidelberg, Germany, 2-3 May 2008. http://genomebiology.com/2008/9/7/314 Rainer Pepperkok and Stefan Wiemann Genome Biology 2008, 9:314 2008-07-01 doi:10.1186/gb-2008-9-7-314 Genome Biology 1465-6906 9 314 2008-07-01 We show that although the currently available isochore mapping methods agree on the isochore classification of about two thirds of the human DNA, they produce significantly different results with regard to the location of isochore boundaries and isochore length distribution. We present a new consensus isochore assignment method based on majority voting and provide IsoBase - a comprehensive on-line database of isochore maps for all completely sequenced vertebrate genomes. http://genomebiology.com/2008/9/6/R104 Thorsten Schmidt and Dmitrij Frishman Genome Biology 2008, 9:R104 2008-06-30 doi:10.1186/gb-2008-9-6-r104 Genome Biology 1465-6906 9 R104 2008-06-30 Metazoans contain multiple complex microbial ecosystems in which the balance between host and microbe can be tipped from commensalism to pathogenicity. This transition is likely to depend both on the prevailing environmental conditions and on specific gene-gene interactions placed within the context of the entire ecosystem. http://genomebiology.com/2008/9/6/225 Garth D Ehrlich, N Luisa Hiller and Fen Ze Hu Genome Biology 2008, 9:225 2008-06-24 doi:10.1186/gb-2008-9-6-225 Genome Biology 1465-6906 9 225 2008-06-24 A response to Combined analysis reveals a core set of cycling genes by Y Lu, S Mahony, PV Benos, R Rosenfeld, I Simon, LL Breeden and Z Bar-Joseph. Genome Biol 2007, 8:R146. http://genomebiology.com/2008/9/6/403 Lars Juhl Jensen, Ulrik de Lichtenberg, Thomas Skøt Jensen, Søren Brunak and Peer Bork Genome Biology 2008, 9:403 2008-06-23 doi:10.1186/gb-2008-9-6-403 Genome Biology 1465-6906 9 403 2008-06-23 We need to familiarize ourselves with the facts of evolution, so that we can mount a spirited defense against creationism and the forces of ignorance. http://genomebiology.com/2008/9/6/106 Gregory A Petsko Genome Biology 2008, 9:106 2008-06-23 doi:10.1186/gb-2008-9-6-106 Genome Biology 1465-6906 9 106 2008-06-23 Background: Trypanosoma brucei is the causative agent of human sleeping sickness and animal trypanosomiasis in sub-Saharan Africa and has been subdivided into three subspecies: Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense, which cause sleeping sickness in humans and the non-human infective Trypanosoma brucei brucei. T.b.gambiense is the most clinically relevant sub-species, responsible for over 90% of all human disease. The genome sequence is now available and a Mendelian genetic system has been demonstrated in T.brucei, facilitating genetic analysis in this diploid protozoan parasite. As an essential step towards identifying loci that determine important traits in the human-infective subspecies, we report the construction of a high-resolution genetic map of the STIB 386 strain of T.b.gambiense. Results: The genetic map was determined using 119 microsatellite markers assigned to the 11 megabase chromosomes. The total genetic map length of the linkage groups was 733.1 centiMorgans covering a physical distance of 17.9 Megabases with an average map unit size of 24 Kilobases per centiMorgan. Forty-seven markers in this map were also used in a genetic map of the non-human infective T.b.brucei subspecies permitting comparison of the two maps and showing that synteny is conserved between the two subspecies. Conclusions: The genetic linkage map presented here is the first available for the human-infective trypanosome, T.b.gambiense. In combination with the genome sequence, this opens up the possibility of using genetic analysis to identify the loci responsible for T.b.gambiense specific traits such as human infectivity as well as comparative studies of parasite field populations. http://genomebiology.com/2008/9/6/R103 Anneli Cooper, Andy Tait, Lindsay Sweeney, Alison Tweedie, Liam Morrison, C Michael R Turner and Annette MacLeod Genome Biology 2008, 9:R103 2008-06-22 doi:10.1186/gb-2008-9-6-r103 Genome Biology 1465-6906 9 R103 2008-06-22 Background: Altered neuronal vulnerability underlies many diseases of the human nervous system, resulting in degeneration and loss of neurons. The neuroprotective Wallerian Degeneration Slow (WldS) mutation delays degeneration in axonal and synaptic compartments of neurons following a wide range of traumatic and disease-inducing stimuli, providing a powerful experimental tool with which to investigate modulation of neuronal vulnerability. Although the mechanisms through which WldS confers neuroprotection remain unclear a diverse range of downstream modifications, incorporating several genes/pathways, have been implicated. These include: elevated NAD levels associated with nicotinamide mononucleotide adenylyltransferase 1 (Nmnat1; a part of the chimeric WldS gene); altered mRNA expression levels of genes such as pituitary tumor transforming gene 1 (Pttg1); changes in the location/activity of the ubiquitin-proteasome machinery via binding to valosin-containing protein (VCP/p97); and modified synaptic expression of proteins such as ubiquitin-activating Enzyme E1 (Ube1). Results: WldS expression in mouse cerebellum and HEK293 cells induced robust increases in a broad spectrum of cell cycle-related genes. Both NAD- and Pttg1-dependent pathways were responsible for mediating different subsets of these alterations, also incorporating changes in VCP/p97 localisation and Ube1 expression. Cell proliferation rates were not modified by WldS, suggesting that later mitotic phases of the cell cycle remained unaltered. We also demonstrate that WldS concurrently altered endogenous cell stress pathways. Conclusions: We report a novel cellular phenotype in cells with altered neuronal vulnerability. We show that previous reports of diverse changes occurring downstream from WldS expression converge upon modifications in cell cycle status. These data suggest a strong correlation between modified cell cycle pathways and altered vulnerability of axonal and synaptic compartments in post-mitotic, terminally differentiated neurons. http://genomebiology.com/2008/9/6/R101 Thomas M Wishart, Helen M Pemberton, Sally R James, Chris J McCabe and Thomas H Gillingwater Genome Biology 2008, 9:R101 2008-06-20 doi:10.1186/gb-2008-9-6-r101 Genome Biology 1465-6906 9 R101 2008-06-20 The Generic Model Organism Database (GMOD) initiative provides species-agnostic data models and software tools for representing curated model organism data. Here we describe GMODWeb, a GMOD project designed to speed the development of Model Organism Database (MOD) websites. Sites created with GMODWeb provide integration with other GMOD tools and allow users to browse and search through a variety of data types. GMODWeb was built using the open source Turnkey web framework and is available from http://turnkey.sourceforge.net. http://genomebiology.com/2008/9/6/R102 Brian D O'Connor, Allen Day, Scott Cain, Olivier Arnaiz, Linda Sperling and Lincoln D Stein Genome Biology 2008, 9:R102 2008-06-20 doi:10.1186/gb-2008-9-6-r102 Genome Biology 1465-6906 9 R102 2008-06-20 This report details the standardized experimental design and the different data streams that were collected (histopathology, clinical chemistry, hematology and gene expression from the target tissue (liver) and a bio-available tissue (blood)) after treatment with eight known hepatotoxicants (at multiple time points and doses with multiple biological replicates). The results of the study demonstrate the classification of histopathological differences, likely reflecting differences in mechanisms of cell-specific toxicity, using either liver tissue or blood transcriptomic data. http://genomebiology.com/2008/9/6/R100 Edward K Lobenhofer, J Todd Auman, Pamela E Blackshear, Gary A Boorman, Pierre R Bushel, Michael L Cunningham, Jennifer M Fostel, Kevin Gerrish, Alexandra N Heinloth, Richard D Irwin, David E Malarkey, B Alex Merrick, Stella O Sieber, Charles J Tucker, Sandra M Ward, Ralph E Wilson, Patrick Hurban, Raymond W Tennant and Richard S Paules Genome Biology 2008, 9:R100 2008-06-20 doi:10.1186/gb-2008-9-6-r100 Genome Biology 1465-6906 9 R100 2008-06-20 A report on the Cold Spring Harbor Laboratory meeting 'Systems Biology: Global Regulation of Gene Expression', Cold Spring Harbor, USA, 27-30 March 2008. http://genomebiology.com/2008/9/6/313 Stein Aerts and Stefanie Butland Genome Biology 2008, 9:313 2008-06-19 doi:10.1186/gb-2008-9-6-313 Genome Biology 1465-6906 9 313 2008-06-19