Specific genes involved in cellular functions or structures are activated or repressed in cells treated with 8-MOP/UVA

<p><b>Copyright information:</b></p><p>Taken from "Specific transcriptional responses induced by 8-methoxypsoralen and UVA in yeast"</p><p></p><p>Fems Yeast Research 2007;7(6):866-878.</p><p>Published online 30 Jul 2007</p><p>PMCID:PMC2040189.</p><p>© 2007 Michèle Dardalhon Journal compilation © 2007 Federation of European Microbiological Societies</p> Plotted data are the mean log ratios. (a) Genes implicated in, cytokinesis, organelle, cytoskeleton, conjugation, meiosis, sporulation, cell wall, and signal transduction. (b) Genes implicated in transcription, homeostasis, and transport. (Genes that fall into multiple categories.

Specific genes involved in cell metabolism are up-regulated or down-regulated in cells treated with 8-MOP/UVA

<p><b>Copyright information:</b></p><p>Taken from "Specific transcriptional responses induced by 8-methoxypsoralen and UVA in yeast"</p><p></p><p>Fems Yeast Research 2007;7(6):866-878.</p><p>Published online 30 Jul 2007</p><p>PMCID:PMC2040189.</p><p>© 2007 Michèle Dardalhon Journal compilation © 2007 Federation of European Microbiological Societies</p> Plotted data are the mean log ratios. (*Genes that fall into multiple categories.

(a) Number and percentage of genes modified by 8-MOP/UVA that are specific to this treatment or that are also induced by other genotoxic agents (details in supplementary )

<p><b>Copyright information:</b></p><p>Taken from "Specific transcriptional responses induced by 8-methoxypsoralen and UVA in yeast"</p><p></p><p>Fems Yeast Research 2007;7(6):866-878.</p><p>Published online 30 Jul 2007</p><p>PMCID:PMC2040189.</p><p>© 2007 Michèle Dardalhon Journal compilation © 2007 Federation of European Microbiological Societies</p> (b) Genes encoding components responding to environmental stress are up- or down-regulated after treatment of cells with 8-MOP/UVA. Plotted data are the mean log ratios. (Genes that fall into multiple categories.

Responses to 8-MOP damage in wild-type cells following treatment with 5 μM 8-MOP plus 5 kJ m UVA as compared to 8-MOP/dark-treated cells (exposure to 5 μM 8-MOP in the dark)

<p><b>Copyright information:</b></p><p>Taken from "Specific transcriptional responses induced by 8-methoxypsoralen and UVA in yeast"</p><p></p><p>Fems Yeast Research 2007;7(6):866-878.</p><p>Published online 30 Jul 2007</p><p>PMCID:PMC2040189.</p><p>© 2007 Michèle Dardalhon Journal compilation © 2007 Federation of European Microbiological Societies</p> Top: growth of 8-MOP/UVA- and 8-MOP/dark-treated cells after posttreatment incubation in complete growth medium. Middle: cell cycle profiles of 8-MOP/UVA- and 8-MOP/dark-treated cells during posttreatment incubation in complete medium as monitored by FACS analysis. C1 denotes a single genome content (equivalent to that of G1 haploids) and C2 denotes a double genome content (equivalent to that of G2 haploids). Bottom: Northern blot analysis of mRNA levels in 8-MOP/UVA- and 8-MOP/dark-treated cells. Induction was normalized to actin () transcript levels and is given in arbitrary units

Time order of food ingestion during the sequential binge (example with 4 binge foods and 4 packages).

<p>Time order of food ingestion during the sequential binge (example with 4 binge foods and 4 packages).</p

Participants’ socio-demographic and clinical characteristics.

<p>Medians (interquartile) are reported, otherwise specified.</p

Stimulation of Gross Chromosomal Rearrangements by the Human CEB1 and CEB25 Minisatellites in <em>Saccharomyces cerevisiae</em> Depends on G-Quadruplexes or Cdc13

<div><p>Genomes contain tandem repeats that are at risk of internal rearrangements and a threat to genome integrity. Here, we investigated the behavior of the human subtelomeric minisatellites HRAS1, CEB1, and CEB25 in <em>Saccharomyces cerevisiae</em>. In mitotically growing wild-type cells, these GC–rich tandem arrays stimulate the rate of gross chromosomal rearrangements (GCR) by 20, 1,620, and 276,000-fold, respectively. In the absence of the Pif1 helicase, known to inhibit GCR by telomere addition and to unwind G-quadruplexes, the GCR rate is further increased in the presence of CEB1, by 385-fold compared to the <em>pif1Δ</em> control strain. The behavior of CEB1 is strongly dependent on its capacity to form G-quadruplexes, since the treatment of WT cells with the Phen-DC₃ G-quadruplex ligand has a 52-fold stimulating effect while the mutation of the G-quadruplex-forming motif reduced the GCR rate 30-fold in WT and 100-fold in <em>pif1Δ</em> cells. The GCR events are telomere additions within CEB1. Differently, the extreme stimulation of CEB25 GCR depends on its affinity for Cdc13, which binds the TG-rich ssDNA telomere overhang. This property confers a biased orientation-dependent behavior to CEB25, while CEB1 and HRAS1 increase GCR similarly in either orientation. Furthermore, we analyzed the minisatellites‚ distribution in the human genome and discuss their potential role to trigger subtelomeric rearrangements.</p> </div

Internal rearrangement frequencies of CEB1 in WT cells treated or not with 10 µM Phen-DC₃, and in <i>pif1Δ</i> cells.

*<p>p-value vs. Control<0.05.</p>°<p>p-value vs. WT<0.05.</p

genotype_files_dryad_for_Laureau_et_al

genotype files from Wild Type 4-spore tetrads and RTG from S288c/SK1 meiosis

The nature of the GCR, but not the GCR rate, depends on the orientation of CEB1 in WT cells.

<p>(A) GCR rates in untreated (grey) and Phen-DC₃-treated (white) WT cells bearing CEB1-WT-1.7 in the orientation G (ORT6542-6) and C (ORT6591-1), and CEB1-Gmut-1.7 in the orientation G (ORT6550-2) and C (ORT6548). The fold increases of the GCR rate upon treatment with Phen-DC₃ is indicated. (B) GCR rates in <i>pif1Δ</i> cells bearing CEB1-WT-1.7 in the orientation G (ORT6543-1) and C (ORT7153-9), and CEB1-Gmut-1.7 in the orientation G (ORT6551-1) and C (ORT6549). The dotted line indicates the GCR rate in the “no minisatellite” control <i>pif1Δ</i> strain (ORT6568) (see <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003033#pgen-1003033-g001" target="_blank">Figure 1D</a>). Other legends as in <a href="http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1003033#pgen-1003033-g001" target="_blank">Figure 1D</a>. (C) The top panel schematically represents the genomic region surrounding CEB1 with the <i>Sac</i>I restriction site and CEB1 (green) and <i>hphMX</i> (blue) probes used to study rearrangements of the region. The size of the unaltered region upon digestion is indicated. The example of a translocation within CEB1 is shown, and is expected to produce a fragment longer than 1.7 kb. The bottom panels show the rearrangements present in 14 5FOA/Can-resistant clones obtained from independent cultures of WT cells bearing CEB1-WT-1.7 in the orientation C, and in the parental 5FOA/Can-sensitive strain (WT, ORT6591-1). In most lanes the bands hybridized both the CEB1 and the <i>hphMX</i> probes, except in clone 9 in which CEB1 has been lost. M = Size marker. (D) Nature of the GCR determined by Southern blot analysis of independent 5FOA/Can-resistant colonies derived of cells bearing CEB1-WT-1.7 in the orientations G or C, in WT cells treated or not with Phen-DC₃ 10 µM, or in <i>pif1Δ</i> cells. The results are presented as a percentage of the total number (n) of 5FOA/Can-resistant colonies analyzed. Telomere additions are shown in red, and their locations relative to CEB1 are indicated by different motifs: within CEB1 (no motif), in proximal (cross), or in distal (lines) position to CEB1. Other rearrangements that appear as discrete bands on the Southern blots are shown in grey: single junction (only one band) and multiple junctions (more than one band) are shown in dark grey and grey, respectively. The strain point mutated for <i>URA3</i> and <i>CAN1</i> (point mutations) is shown in light grey. In some instances, colonies have lost both CEB1 and <i>hphMX</i> and the junction has not been determined (Undetermined, white): this may correspond to telomere additions or other rearrangements in the 8.3 kb region between <i>hphMX</i> and the first essential gene (<i>PCM1</i>). Distributions were compared using the Fisher's exact test.</p