Expression domains of common response genes and symptoms associated with infection

GFP. In contrast, no GFP expression or vacuolization was seen in the intestines of non-infected worms.<p><b>Copyright information:</b></p><p>Taken from "Genome-wide investigation reveals pathogen-specific and shared signatures in the response of to infection"</p><p>http://genomebiology.com/2007/8/9/R194</p><p>Genome Biology 2007;8(9):R194-R194.</p><p>Published online 17 Sep 2007</p><p>PMCID:PMC2375032.</p><p></p

Comparison of host gene expression profiles following infection with different pathogens

Expression levels are indicated by a color scale and represent normalized differences between infected and control animals. Grey denotes genes not considered to be differentially regulated under that condition. The numbers on the vertical axis correspond to differentially regulated genes. Each column shows the expression levels of individual genes (represented as rows) following infection by the pathogens as indicated on the horizontal axis (, ; , ; , ; , ). Genes differentially regulated in an infection with and their comparative expression levels with other pathogens. Genes defining a pathogen-specific signature specifically up-regulated with infection. Groupings, as indicated by the horizontal bars, formed after clustering using non-redundant sets of genes that were up- and down-regulated by at least two pathogens (trees not shown). Genes commonly up-regulated following , and infections.<p><b>Copyright information:</b></p><p>Taken from "Genome-wide investigation reveals pathogen-specific and shared signatures in the response of to infection"</p><p>http://genomebiology.com/2007/8/9/R194</p><p>Genome Biology 2007;8(9):R194-R194.</p><p>Published online 17 Sep 2007</p><p>PMCID:PMC2375032.</p><p></p

The <i>nipi-4</i> gene acts cell autonomously in the epidermis.

<p>(A–E) Expression of <i>nipi-4</i> is seen throughout the epidermis (A & B)), in larvae (C) and adults (A,B,D&E), from head (D) to tail (E), in vulval cells (arrow in B), in rectal cells (arrow in E), but not in the seam cells (arrowhead in A), scale bar 10 µm. (F–G) <i>nipi-4</i>(<i>fr71</i>) and <i>nipi-4</i>(<i>fr71</i>);<i>frEx496</i> (P<i>col-19</i>::NIPI-4) worms strains carrying an integrated P<i>nlp-29</i>::GFP reporter (<i>frIs7</i>) following infection. The expression of <i>nipi-4</i> in epidermal cells in the adult rescues the <i>nipi-4</i> phenotype. Green and red fluorescence is visualized simultaneously with a GFP long pass filter.</p

New Nipi alleles isolated in a large scale screen.

<p>(A) Biosort quantification of the fluorescence in wild type and different mutants strains carrying an integrated P<i>nlp-29</i>::GFP reporter (<i>frIs7</i>) following infection including <i>sta-2(ok1860)</i>, <i>nipi-3(fr4)</i>, <i>tpa-1(k530)</i> and 38 new alleles, 11 of which have been determined to define 6 new independent complementation groups. The average fold induction for each strain is represented after standardization across different independent experiments by normalizing to 10 the fold induction between the wild type strain infected versus non infected. (B) Genetic map of Nipi loci identified from screens or from candidate gene approaches. The map has been scaled to the genome sequence, as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033887#pone.0033887-Yook1" target="_blank">[48]</a>. The Nipi genes identified in the present mutagenesis and in previous studies <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033887#pone.0033887-Couillault1" target="_blank">[15]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033887#pone.0033887-Pujol3" target="_blank">[18]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033887#pone.0033887-Ziegler1" target="_blank">[20]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033887#pone.0033887-Dierking1" target="_blank">[21]</a> (Couillault <i>et al.</i> submitted) are represented in red and black respectively.</p

<i>nipi-4</i> encodes a pseudokinase required for the induction of <i>nlp-29</i>.

<p>(A) SNP mapping with WGS. The positions of SNP loci on Chromosome V for the <i>fr106</i> allele are depicted as a XY scatter plot, where the ratio ‘Hawaiian/total number of reads’ for each SNP is represented, as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033887#pone.0033887-Doitsidou1" target="_blank">[35]</a>. The region without Hawaiian SNPs contains the mutation (red arrow). (B) Exon-intron structure of <i>nipi-4</i>, adapted from WormBase (WS220), with the positions of the <i>fr68</i>, <i>fr71</i>, <i>fr99</i> and <i>fr106</i> mutations indicated. Also shown is the structure of the p<i>nipi-4</i>::GFP & p<i>nipi-4</i>::NIPI-4 constructs. (C) Biosort quantification of the normalized fluorescence ratio in wild type, <i>sta-2(ok1860)</i> and the 4 <i>nipi-4</i> alleles <i>fr68</i>, <i>fr71</i>, <i>fr99</i> and <i>fr106</i> carrying <i>frIs7</i> following infection. For this and subsequent figures, see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033887#s4" target="_blank">Materials and Methods</a> for details of the data processing and the number of worms analyzed. The results are representative of 3 independent experiments. (D) Biosort quantification of the normalized fluorescence ratio in wild type, <i>nipi-4(fr106)</i> and <i>nipi-4(fr106)</i> with a rescuing transgene p<i>nipi-4</i>::NIPI-4, carrying <i>frIs7</i> following infection.</p

New Nipi alleles.

1<p>WormBase Release WS228.</p

The <i>nipi-4</i> gene is required for the response to infection and wounding.

<p>(A) <i>nipi-4</i> mutants do not block the induction of <i>nlp-29</i> expression upon osmotic stress. Biosort quantification of the normalized fluorescence ratio in wild type, <i>sta-2(ok1860)</i> and <i>nipi-4(fr71)</i> worms carrying <i>frIs7</i> following infection by <i>D. coniospora</i>, wounding, PMA treatment and osmotic stress. (B) Quantitative RT-PCR analysis of gene expression levels in non- infected and infected wild type, <i>sta-2(ok1860)</i> and <i>nipi-4(fr106)</i> worms. The columns show the average expression level (arbitrary units) and SEM from 4 experiments. The level of <i>nlp-34</i> expression in control animals is set at 1024 (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0033887#s4" target="_blank">Materials and Methods</a>).</p

Additional file 10: Figure S9. of Coordinated inhibition of C/EBP by Tribbles in multiple tissues is essential for Caenorhabditis elegans development

Hierarchical clustering of genes and functional classes. The presence of a gene in a class is represented by a red rectangle, its absence in blue. See Additional file 8: Table S1 for class labels and full data. (PDF 680 kb

Additional file 12: Table S3. of Coordinated inhibition of C/EBP by Tribbles in multiple tissues is essential for Caenorhabditis elegans development

List of plasmids and primers used for qRT-PCR. (XLSX 13 kb

The metaphysical thought of Thomas Aquinas. From the concept of being and unity to the concept of whole and part

The subject-matter of the thesis is the metaphysical thought of the renowned medieval philosopher and theologian Thomas Aquinas (1224/5-1274). The main goal ofthe thesis is to expose Aquinas' part-whole doctrine (mereology) in the broad context of his metaphysical theory. In concrete, we mean to elucidate the part-whole relationship in the background ofthe key metaphysical principles and concepts, such as the notion of being and unity or the issue of the ontological structure of a categorial being. The whole thesis can be divided into two main parts. In the first part we tackle those issues, which must be outlined to comprehend Aquinas' mereology in the broad horizon of his metaphysics. In the second part we set forth the independent attempt to advance Aquinas' part-whole theory