Rice Galaxy: An open resource for plant science

Background: Rice molecular genetics, breeding, genetic diversity, and allied research (such as rice-pathogen interaction) have adopted sequencing technologies and high-density genotyping platforms for genome variation analysis and gene discovery. Germplasm collections representing rice diversity, improved varieties, and elite breeding materials are accessible through rice gene banks for use in research and breeding, with many having genome sequences and high-density genotype data available. Combining phenotypic and genotypic information on these accessions enables genome-wide association analysis, which is driving quantitative trait loci discovery and molecular marker development. Comparative sequence analyses across quantitative trait loci regions facilitate the discovery of novel alleles. Analyses involving DNA sequences and large genotyping matrices for thousands of samples, however, pose a challenge to non−computer savvy rice researchers. Findings: The Rice Galaxy resource has shared datasets that include high-density genotypes from the 3,000 Rice Genomes project and sequences with corresponding annotations from 9 published rice genomes. The Rice Galaxy web server and deployment installer includes tools for designing single-nucleotide polymorphism assays, analyzing genome-wide association studies, population diversity, rice−bacterial pathogen diagnostics, and a suite of published genomic prediction methods. A prototype Rice Galaxy compliant to Open Access, Open Data, and Findable, Accessible, Interoperable, and Reproducible principles is also presented. Conclusions: Rice Galaxy is a freely available resource that empowers the plant research community to perform state-of-the-art analyses and utilize publicly available big datasets for both fundamental and applied science

Physiological evaluation of free-ranging moose (<it>Alces alces</it>) immobilized with etorphine-xylazine-acepromazine in Northern Sweden

<p>Abstract</p> <p>Background</p> <p>Evaluation of physiology during capture and anesthesia of free-ranging wildlife is useful for determining the effect that capture methods have on both ecological research results and animal welfare. This study evaluates capture and anesthesia of moose (<it>Alces alces</it>) with etorphine-xylazine-acepromazine in Northern Sweden.</p> <p>Methods</p> <p>Fifteen adult moose aged 3–15 years were darted from a helicopter with a combination of 3.37 mg etorphine, 75 mg xylazine, and 15 mg acepromazine. Paired arterial blood samples were collected 15 minutes apart with the first sample at 15–23 minutes after darting and were analyzed immediately with an i-STAT®1 Portable Clinical Analyzer.</p> <p>Results</p> <p>All animals developed hypoxemia (PaO₂ <10 kPa) with nine animals having marked hypoxemia (PaO₂ 5.5-8 kPa). All moose were acidemic (ph<7.35) with nine moose having marked acidemia (pH<7.20). For PaCO_2, 14 moose had mild hypercapnia (PaCO₂ 6-8 kPa) and two had marked hypercapnia (PaCO₂>8 kPa). Pulse, respiratory rate, pH and HCO₃ increased significantly over time from darting whereas lactate decreased.</p> <p>Conclusions</p> <p>The hypoxemia found in this study is a strong indication for investigating alternative drug doses or combinations or treatment with supplemental oxygen.</p

Maximal killing of lymphoma cells by DNA damage–inducing therapy requires not only the p53 targets Puma and Noxa, but also Bim

DNA-damaging chemotherapy is the backbone of cancer treatment, although it is not clear how such treatments kill tumor cells. In nontransformed lymphoid cells, the combined loss of 2 proapoptotic p53 target genes, Puma and Noxa, induces as much resistance to DNA damage as loss of p53 itself. In Eμ-Myc lymphomas, however, lack of both Puma and Noxa resulted in no greater drug resistance than lack of Puma alone. A third B-cell lymphoma-2 homology domain (BH)3-only gene, Bim, although not a direct p53 target, was up-regulated in Eμ-Myc lymphomas incurring DNA damage, and knockdown of Bim levels markedly increased the drug resistance of Eμ-Myc/Puma−/−Noxa−/− lymphomas both in vitro and in vivo. Remarkably, c-MYC–driven lymphoma cell lines from Noxa−/−Puma−/−Bim−/− mice were as resistant as those lacking p53. Thus, the combinatorial action of Puma, Noxa, and Bim is critical for optimal apoptotic responses of lymphoma cells to 2 commonly used DNA-damaging chemotherapeutic agents, identifying Bim as an additional biomarker for treatment outcome in the clinic