12 research outputs found
Literature-aided meta-analysis of microarray data: a compendium study on muscle development and disease-2
Ddition to relevant subclusters. The dataset ids are shown between the tree and the heatmap. The colored bars provide background information on the datasets.<p><b>Copyright information:</b></p><p>Taken from "Literature-aided meta-analysis of microarray data: a compendium study on muscle development and disease"</p><p>http://www.biomedcentral.com/1471-2105/9/291</p><p>BMC Bioinformatics 2008;9():291-291.</p><p>Published online 24 Jun 2008</p><p>PMCID:PMC2459190.</p><p></p
Literature-aided meta-analysis of microarray data: a compendium study on muscle development and disease-0
<p><b>Copyright information:</b></p><p>Taken from "Literature-aided meta-analysis of microarray data: a compendium study on muscle development and disease"</p><p>http://www.biomedcentral.com/1471-2105/9/291</p><p>BMC Bioinformatics 2008;9():291-291.</p><p>Published online 24 Jun 2008</p><p>PMCID:PMC2459190.</p><p></p
Literature-aided meta-analysis of microarray data: a compendium study on muscle development and disease-1
level.<p><b>Copyright information:</b></p><p>Taken from "Literature-aided meta-analysis of microarray data: a compendium study on muscle development and disease"</p><p>http://www.biomedcentral.com/1471-2105/9/291</p><p>BMC Bioinformatics 2008;9():291-291.</p><p>Published online 24 Jun 2008</p><p>PMCID:PMC2459190.</p><p></p
Literature-aided meta-analysis of microarray data: a compendium study on muscle development and disease-3
Ion to relevat subclusters. The dataset ids are shown between the tree and the heatmap. The colored bars provide background information on the datasets.<p><b>Copyright information:</b></p><p>Taken from "Literature-aided meta-analysis of microarray data: a compendium study on muscle development and disease"</p><p>http://www.biomedcentral.com/1471-2105/9/291</p><p>BMC Bioinformatics 2008;9():291-291.</p><p>Published online 24 Jun 2008</p><p>PMCID:PMC2459190.</p><p></p
Adaptive pathways are involved in cell cycle, DNA repair and protoporphyrinogen metabolism.
<p>Shown is the sub-network that prioritizes putative adaptive mutations by applying PheNetic on all selected mutations, excluding those originating from the populations with a mutator phenotype i.e. reactor 2 and 6. The nodes in the network correspond to genes and/or their associated gene products. Node borders are colored according to the reactors containing the populations in which these genes were mutated. Nodes are colored according to gene function, for each gene the most enriched term is visualized (grey indicates no enrichment). Cell cycle related processes have been subdivided into DNA replication and interphase. The edge colors indicate different interaction types. Orange lines represent metabolic interactions, green lines represent protein-protein interactions, red lines represent protein-DNA interactions. Sub-networks extracted by separately analyzing the mutated genes observed in each of the different populations (reactors) are shown in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005635#pgen.1005635.s008" target="_blank">S8</a>–<a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005635#pgen.1005635.s013" target="_blank">S13</a> Figs.</p
Haploid lineages diploidized during adaptation to EtOH.
<p>Flow cytometry analysis of DNA content (stained by propidium iodide) of evolved populations, compared to ancestral haploid (red) and diploid (blue). For the clonal ancestral samples, two peaks are observed, corresponding to the G1 and G2 phase of the cell cycle. Evolved populations sometimes display three peaks, indicative of both haploid and diploid subpopulations.</p
Dynamics and linkage of mutations in evolved populations of reactor 2.
<p>Mutations (reaching a frequency of least 20% in the evolved population samples) and corresponding frequencies were identified from population sequencing data. Muller diagram represents the hierarchical clustering of these mutations, with each color block representing a specific group of linked mutations. Indels are designated with <sup>I</sup>, whereas heterozygous mutations are in italics. Mutations present as heterozygous mutations in all clones of a specific time point and present at a frequency of 50% in the population, are depicted as a frequency of 100% in the population, since it is expected that all cells in the population contain this mutation. After 80 generations, a mutator phenotype appeared in this reactor (indicated by arrow under graph), which coincides with the rise in frequency of an indel in the mismatch repair gene <i>MSH2</i>. Frequencies of haplotypes can be found in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005635#pgen.1005635.s026" target="_blank">S2 Table</a>. Dynamics and linkage for reactor 1 is shown in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005635#pgen.1005635.s007" target="_blank">S7 Fig</a>.</p
SNPs in evolved lineages selected for introduction in non-ethanol tolerant strain.
<p>*Enriched process identified by Phenetic analyses across all reactors</p><p>SNPs reaching high frequencies in the different evolved lineages were introduced in a haploid, non-ethanol tolerant strain. Gene functions were obtained from SGD, <a href="http://www.yeastgenome.org" target="_blank">http://www.yeastgenome.org</a>.</p
Experimental setup.
<p>(A) Experimental evolution of prototrophic, isogenic populations of different ploidy (haploid (VK111), diploid (VK145) and tetraploid (VK202)) for increased ethanol tolerance was performed in a turbidostat. Every 25 generations, the ethanol concentration in the media was increased in a stepwise manner (starting at 6% (v/v) and reaching 12% at 200 generations). Increasing the ethanol concentration from 10% to 11% dramatically reduced growth rate of evolving cells. Therefore, instead of increasing ethanol levels, we first reduced the ethanol level to 10.7% after 100 generations. (B) Red circles represent sampling points (indicated as number of generations) for which whole-genome sequencing was performed. For each circle, heterogeneous populations as well as three evolved, ethanol tolerant clones were sequenced. Sequencing of the population sample of reactor 4 at 200 generations failed, so this data is omitted from the manuscript. For generation 80 of reactor 1, only population data is available.</p
Single mutations present in evolved populations can increase ethanol tolerance of a non-adapted strain.
<p>Plots show the average selection coefficient (<i>s</i><sub>mut</sub>) as a function of ethanol concentration for (<b>A</b>) <i>pca1</i><sup><i>C1583T</i></sup>, (<b>B</b>) <i>prt1</i><sup><i>A1384G</i></sup>, (<b>C</b>) <i>ybl059w</i><sup><i>G479T</i></sup>, (<b>D</b>) <i>intergenic ChrIV A1489310T</i>, (<b>E</b>) <i>hem13</i><sup><i>G700C</i></sup>, (<b>F</b>) <i>intergenic ChrXII C747403T</i>, (<b>G</b>) <i>hst4</i><sup><i>G262C</i></sup>, (<b>H</b>) <i>vps70</i><sup><i>C595A</i></sup>, and (<b>I</b>) <i>mex67</i><sup><i>G456A</i></sup>. Superscripts denote the exact nucleotide change in each of the mutants tested. YECitrine-tagged mutants were competed with the mCherry-tagged parental strain (orange dots); dye-swap experiments were carried out by competing the mCherry-tagged mutants with the YECitrine parental strain (blue dots), except for (<b>I</b>). Error bars show the S.E.M. from three experimental replicates. Asterisk show P-values from the one-way ANOVA tests of the mean differences in 4–8% ethanol compared to fitness in 0% ethanol: * <i>p</i> < 0.05; ** <i>p</i> < 0.01; ***<i>p</i> < 0.005. P values can be found in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1005635#pgen.1005635.s031" target="_blank">S7 Table</a>.</p