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  • 1
    Publication Date: 2011-09-17
    Description: Structural variation is widespread in mammalian genomes and is an important cause of disease, but just how abundant and important structural variants (SVs) are in shaping phenotypic variation remains unclear. Without knowing how many SVs there are, and how they arise, it is difficult to discover what they do. Combining experimental with automated analyses, we identified 711,920 SVs at 281,243 sites in the genomes of thirteen classical and four wild-derived inbred mouse strains. The majority of SVs are less than 1 kilobase in size and 98% are deletions or insertions. The breakpoints of 160,000 SVs were mapped to base pair resolution, allowing us to infer that insertion of retrotransposons causes more than half of SVs. Yet, despite their prevalence, SVs are less likely than other sequence variants to cause gene expression or quantitative phenotypic variation. We identified 24 SVs that disrupt coding exons, acting as rare variants of large effect on gene function. One-third of the genes so affected have immunological functions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428933/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3428933/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yalcin, Binnaz -- Wong, Kim -- Agam, Avigail -- Goodson, Martin -- Keane, Thomas M -- Gan, Xiangchao -- Nellaker, Christoffer -- Goodstadt, Leo -- Nicod, Jerome -- Bhomra, Amarjit -- Hernandez-Pliego, Polinka -- Whitley, Helen -- Cleak, James -- Dutton, Rebekah -- Janowitz, Deborah -- Mott, Richard -- Adams, David J -- Flint, Jonathan -- 079912/Wellcome Trust/United Kingdom -- 082356/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 098051/Wellcome Trust/United Kingdom -- 13031/Cancer Research UK/United Kingdom -- G0800024/Medical Research Council/United Kingdom -- MC_U137761446/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- England -- Nature. 2011 Sep 14;477(7364):326-9. doi: 10.1038/nature10432.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust Centre for Human Genetics, Roosevelt Drive, Oxford OX3 7BN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921916" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Breakpoints ; Exons/genetics ; Female ; Gene Expression ; Genetic Variation/*genetics ; Genome/*genetics ; Genomics ; Genotype ; Male ; Mice ; Mice, Inbred Strains/*genetics/immunology ; Mutagenesis, Insertional/genetics ; *Phenotype ; Quantitative Trait Loci/genetics ; Rats ; Retroelements/genetics ; Sequence Deletion/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2011-09-17
    Description: We report genome sequences of 17 inbred strains of laboratory mice and identify almost ten times more variants than previously known. We use these genomes to explore the phylogenetic history of the laboratory mouse and to examine the functional consequences of allele-specific variation on transcript abundance, revealing that at least 12% of transcripts show a significant tissue-specific expression bias. By identifying candidate functional variants at 718 quantitative trait loci we show that the molecular nature of functional variants and their position relative to genes vary according to the effect size of the locus. These sequences provide a starting point for a new era in the functional analysis of a key model organism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276836/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276836/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keane, Thomas M -- Goodstadt, Leo -- Danecek, Petr -- White, Michael A -- Wong, Kim -- Yalcin, Binnaz -- Heger, Andreas -- Agam, Avigail -- Slater, Guy -- Goodson, Martin -- Furlotte, Nicholas A -- Eskin, Eleazar -- Nellaker, Christoffer -- Whitley, Helen -- Cleak, James -- Janowitz, Deborah -- Hernandez-Pliego, Polinka -- Edwards, Andrew -- Belgard, T Grant -- Oliver, Peter L -- McIntyre, Rebecca E -- Bhomra, Amarjit -- Nicod, Jerome -- Gan, Xiangchao -- Yuan, Wei -- van der Weyden, Louise -- Steward, Charles A -- Bala, Sendu -- Stalker, Jim -- Mott, Richard -- Durbin, Richard -- Jackson, Ian J -- Czechanski, Anne -- Guerra-Assuncao, Jose Afonso -- Donahue, Leah Rae -- Reinholdt, Laura G -- Payseur, Bret A -- Ponting, Chris P -- Birney, Ewan -- Flint, Jonathan -- Adams, David J -- 077192/Wellcome Trust/United Kingdom -- 079912/Wellcome Trust/United Kingdom -- 082356/Wellcome Trust/United Kingdom -- 083573/Wellcome Trust/United Kingdom -- 083573/Z/07/Z/Wellcome Trust/United Kingdom -- 085906/Wellcome Trust/United Kingdom -- 085906/Z/08/Z/Wellcome Trust/United Kingdom -- 090532/Wellcome Trust/United Kingdom -- 2T15LM007359/LM/NLM NIH HHS/ -- A6997/Cancer Research UK/United Kingdom -- BB/F022697/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0800024/Medical Research Council/United Kingdom -- K25 HL080079/HL/NHLBI NIH HHS/ -- MC_U127561112/Medical Research Council/United Kingdom -- MC_U137761446/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- Medical Research Council/United Kingdom -- England -- Nature. 2011 Sep 14;477(7364):289-94. doi: 10.1038/nature10413.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1HH, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21921910" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Animals, Laboratory/genetics ; Gene Expression Regulation/*genetics ; Genetic Variation/*genetics ; Genome/*genetics ; Genomics ; Mice/classification/*genetics ; Mice, Inbred C57BL/genetics ; Mice, Inbred Strains/*genetics ; *Phenotype ; Phylogeny ; Quantitative Trait Loci/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Macmillan Magazines Ltd.
    Nature 404 (2000), S. 142-143 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Coral reefs are under threat from the effects of bleaching, in which symbiotic algae or their photosynthetic pigments are destroyed by increased sea temperatures and solar radiation. Here we show that the bleaching susceptibility of Goniastrea aspera, a shallow-water Indo-Pacific coral, ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Marine biology 124 (1995), S. 185-195 
    ISSN: 1432-1793
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The size, fecundity and gonad development of Maurplicus muelleri (Gmelin) were studied in Herdlefjorden, western Norway, from January to June 1994. In January, the two age groups formed separate sound-scattering layers (SSL). Juvenile 1-group fish were found to form the upper SSL, while adult 2+ individuals inhabited the lower, these distributions reflecting the different feeding to fitness functions of these two age groups. In June there was only one SSL, and in March and May some 2+ were also found in the upper SSL. Growth of the younger fish to 2+ fish size was observed over the period, and it was found that M. muelleri mature after 1 yr, although size at maturity was lower than found in previous studies. Growth of the 2+ fish changed as the period progressed, to allow gonadal development after a winter of low feeding. Increased investment in development of the gonads was also observed in the 1-group fish over the study period, but substantial maturation only occurred from May to June. Absolute fecundity was size dependent, although high variability was found in the larger size ranges. Oocyte development occurred in discrete batches, although lack of gonadal synchrony between individuals means that spawning is continuous in the population as a whole, once the spawning period begins. Batch fecundity was found to be similar to previous studies, and 2+ fish were found to start spawning earlier, and with an increased intensity, than the 1-group fish.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1420-9071
    Keywords: Escherichia coli ; ColV plasmid ; inhibitory agents ; environmental inhibitors, sensitivity to
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Derivatives ofEscherichia coli carrying the virulence plasmid, ColV, I-K94 were more resistant than the ColV− parents to phage Mel but were more sensitive to the hydrophobic inhibitors deoxycholate, erythromycin and lysozyme. The basis for these changes in sensitivity has been examined in ColV+ mutants with altered colicin or VmpA protein levels and in ColV+ strains with repressed transfer properties.
    Type of Medium: Electronic Resource
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