Selection against tandem splice sites affecting structured protein regions-4

Isk (RR) indicating how much more likely the creation of an implausible NAGNAG is compared to the creation of a plausible NAGNAG is given above the columns. P-values of the CMH test are indicated as ***: P < 0.0001, **: P < 0.001, *: P < 0.01.<p><b>Copyright information:</b></p><p>Taken from "Selection against tandem splice sites affecting structured protein regions"</p><p>http://www.biomedcentral.com/1471-2148/8/89</p><p>BMC Evolutionary Biology 2008;8():89-89.</p><p>Published online 21 Mar 2008</p><p>PMCID:PMC2279118.</p><p></p

Selection against tandem splice sites affecting structured protein regions-1

Ns with tandem donors and acceptors (A) in alpha-helices, beta-sheets, and non-regular elements, (B) 'inside' or 'outside' structural elements (see text), (C) with respect to the average surface accessibility, and (D) with respect to the average inverse hydropathy scores. Kyte-Doolittle values were used to compute hydropathy scores for the ± 5 amino acid contexts. The values were inverted so that positive values indicate polar residues. To avoid potential biases, we excluded the insertion sequence of tandem donors and acceptors from the context. Different context lengths of ± 3, ± 10, or ± 15 residues give consistent results in D (Additional File ). P-values using a χtest in A and B and a Wilcoxon rank sum test in C and D are indicated as *: P < 0.05, **: P < 0.001, ***: P < 0.0001.<p><b>Copyright information:</b></p><p>Taken from "Selection against tandem splice sites affecting structured protein regions"</p><p>http://www.biomedcentral.com/1471-2148/8/89</p><p>BMC Evolutionary Biology 2008;8():89-89.</p><p>Published online 21 Mar 2008</p><p>PMCID:PMC2279118.</p><p></p

Selection against tandem splice sites affecting structured protein regions-3

Dered regions.<p><b>Copyright information:</b></p><p>Taken from "Selection against tandem splice sites affecting structured protein regions"</p><p>http://www.biomedcentral.com/1471-2148/8/89</p><p>BMC Evolutionary Biology 2008;8():89-89.</p><p>Published online 21 Mar 2008</p><p>PMCID:PMC2279118.</p><p></p

Polymorphisms in the mitochondrial genome.

<p>Single nucleotide polymorphisms (SNPs) were counted in a sliding window of 500 with a step size of 1. All genes are depicted below the SNP frequency curve. The indel regions are indicated by vertical lines below the sliding window curve. Protein coding genes (CDS) are shown above the second line and RNA species below that same line as boxes. The CDS and the 12S and 16S RNA genes are named, while the tRNA genes are only depicted as rectangles. The bar-bell shapes indicate the amplified regions from 17 specimen.</p

Molecular Phylogenetic analysis of the concatenated nucleotide sequences from three regions of the mitochondrial genome (2470 to 3050; 5490 to 6890; 12230 to 13380) using the Maximum Likelihood method based on the Hasegawa-Kishino-Yano model [40].

<p>Initial tree(s) for the heuristic search were obtained automatically by applying Neighbor-Join and BioNJ algorithms to a matrix of pairwise distances estimated using the Maximum Composite Likelihood (MCL) approach, and then selecting the topology with superior log likelihood value. The tree is drawn to scale, with branch lengths measured in the number of substitutions per site. Evolutionary analyses were conducted in MEGA5 [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0082857#B38" target="_blank">38</a>]. Blue: Iceland; Green: Baltic Sea; Red: North Sea.</p

Map of the mitochondrial genome of <i>A. islandica</i>.

<p>The image was prepared using the CGView Server at <a href="http://stothard.afns.ualberta.ca/cgi-bin/cgview_server/" target="_blank"><u>http://stothard.afns.ualberta.ca/cgi-bin/cgview_server/</u></a>. The Outer circle shows the genes, the middle circle the GC content and the inner circle the GC skew. </p

Selection against tandem splice sites affecting structured protein regions-2

location in ordered or disordered regions. Each bar is the percentage of introns having a plausible (blue) or implausible (green) NAGNAG acceptor. Absolute intron numbers are given above the bars.<p><b>Copyright information:</b></p><p>Taken from "Selection against tandem splice sites affecting structured protein regions"</p><p>http://www.biomedcentral.com/1471-2148/8/89</p><p>BMC Evolutionary Biology 2008;8():89-89.</p><p>Published online 21 Mar 2008</p><p>PMCID:PMC2279118.</p><p></p

Extension of Life Span by Impaired Glucose Metabolism in <i>Caenorhabditis elegans</i> Is Accompanied by Structural Rearrangements of the Transcriptomic Network

<div><p>Glucose restriction mimicked by feeding the roundworm <i>Caenorhabditis elegans</i> with 2-deoxy-D-glucose (DOG) - a glucose molecule that lacks the ability to undergo glycolysis - has been found to increase the life span of the nematodes considerably. To facilitate understanding of the molecular mechanisms behind this life extension, we analyzed transcriptomes of DOG-treated and untreated roundworms obtained by RNA-seq at different ages. We found that, depending on age, DOG changes the magnitude of the expression values of about 2 to 24 percent of the genes significantly, although our results reveal that the gross changes introduced by DOG are small compared to the age-induced changes. We found that 27 genes are constantly either up- or down-regulated by DOG over the whole life span, among them several members of the cytochrome P450 family. The monotonic change with age of the temporal expression patterns of the genes was investigated, leading to the result that 21 genes reverse their monotonic behaviour under impaired glycolysis. Put simply, the DOG-treatment reduces the gross transcriptional activity but increases the interconnectedness of gene expression. However, a detailed analysis of network parameters discloses that the introduced changes differ remarkably between individual signalling pathways. We found a reorganization of the hubs of the mTOR pathway when standard diet is replaced by DOG feeding. By constructing correlation based difference networks, we identified those signalling pathways that are most vigorously changed by impaired glycolysis. Taken together, we have found a number of genes and pathways that are potentially involved in the DOG-driven extension of life span of <i>C. elegans</i>. Furthermore, our results demonstrate how the network structure of ageing-relevant signalling pathways is reorganised under impaired glycolysis.</p></div

Additional file 4: Table S3. of Hormetic effect of rotenone in primary human fibroblasts

Up-regulated pathways in human foreskin fibroblasts on low dose rotenone treatment. Pathways significantly (p < 0.05) up-regulated on low dose rotenone treatment in one of the three PDs (26, 30 and 34) in HFFs. (DOCX 27 kb

The temporal expression profiles of four genes encoding antioxidant enzymes.

<p>The plot shows the mean RPKM values as well as the standard deviation versus age in days for superoxide dismutase <i>sod-2</i>, the peroxisomal catalase <i>ctl-2</i> and two genes encoding glutathione peroxidases. Black curve: controls; red curve: DOG-treatment.</p