Duplicate gene evolution and expression in the wake of vertebrate allopolyploidization-0

) Regression of Ka/Ks versus Ks in the early and later stages indicates that selection (relaxed purifying + positive) is not more common in the early stage of duplicate gene evolution (blue dots) than the later stage (red dots). The Y-intercept of these regression lines was set to zero and Ka/Ks ratios greater 2 (including undefined ratios) were given a value of 2. In (A) and (B), a dashed line indicates the neutral expectation. Fragments with Ka/Ks > 2 are, on average, half of the size of those with Ka/Ks < 2. Ka/Ks ratios above 2 may therefore be attributable in part to stochastic variance in Ks [43].<p><b>Copyright information:</b></p><p>Taken from "Duplicate gene evolution and expression in the wake of vertebrate allopolyploidization"</p><p>http://www.biomedcentral.com/1471-2148/8/43</p><p>BMC Evolutionary Biology 2008;8():43-43.</p><p>Published online 8 Feb 2008</p><p>PMCID:PMC2275784.</p><p></p

Duplicate gene evolution and expression in the wake of vertebrate allopolyploidization-2

Ofiles (white bars) and between paralogous expression profiles (black bars). Ninety percent of the non-paralogous expression profiles have a Pearson correlation coefficient that is greater than -0.861 but less than 0.865. The Pearson correlation coefficients of 62% of the paralogous expression profiles are less than 0.865, and 0.3% of them are less than -0.861.<p><b>Copyright information:</b></p><p>Taken from "Duplicate gene evolution and expression in the wake of vertebrate allopolyploidization"</p><p>http://www.biomedcentral.com/1471-2148/8/43</p><p>BMC Evolutionary Biology 2008;8():43-43.</p><p>Published online 8 Feb 2008</p><p>PMCID:PMC2275784.</p><p></p

Duplicate gene evolution and expression in the wake of vertebrate allopolyploidization-1

Ction of expression and three probe specificities were compared that are labeled low, medium, and high (see Methods). We report paralogous profiles whose presence/absence scores in all five treatments were identical in the medium and high specificity analysis (shaded in gray on the left of each chart). 1789 and 1462 genes had consistent present/absent expression profiles in the medium and high specificity analyses using the standard and conservative thresholds. These sets of genes included 841 and 632 paralogous pairs, respectively. The tables on the right compare paralogous profiles by tabulating whether they are both present and absent in the same treatments (identical), the expression profile of one overlaps entirely with the other (overlap), or paralogs in which each duplicate has a unique component (distinct).<p><b>Copyright information:</b></p><p>Taken from "Duplicate gene evolution and expression in the wake of vertebrate allopolyploidization"</p><p>http://www.biomedcentral.com/1471-2148/8/43</p><p>BMC Evolutionary Biology 2008;8():43-43.</p><p>Published online 8 Feb 2008</p><p>PMCID:PMC2275784.</p><p></p

PKF118–310 selectively targets breast TICs <i>in</i> vitro.

<p>A) PKF118–310 inhibits sphere formation by primary mammary epithelial cells. B) PKF118–310 inhibits sphere formation by primary tumor cells. C) PKF118–310 treated primary mammary epithelial cells form spheres with same efficiency compared to the DMSO vehicle. D) PKF118–310 treated primary tumor cells have little capacity to form spheres compared to the DMSO vehicle (* p<0.05, t-test). E) Mass (g) of tumors formed from transplant of 1 µM PKF118–310-treated primary tumor cells (* p<0.05, t-test). F) Primary tumor cells treated with 2.5 µM PKF118–310 are unable to initiate tumor growth after transplant into syngeneic recipient mice.</p

Wnt/β-catenin pathway genes comprising the gene signature of differentially expressed genes between tumorspheres and mammospheres induced to differentiate.

<p>Genes shown are those that were differentially expressed between tumorspheres and mammospheres induced to differentiate, as assessed by RT-PCR, and were also present in the NKI dataset.</p

Tumor cells from PKF118–310 treated tumor-bearing mice engraft and elicit the growth of secondary tumors less efficiently than their vehicle-treated counterparts.

<p>Viable tumor cells were harvested from PKF118–310- and DMSO-treated mice and 10,000 viable tumor cells per mouse were transplanted into syngeneic recipients (n = 20 treated/untreated) (* p<0.05, Log-rank test).</p

IC₅₀ values (µM) for PKF118–310, PKF115–584, and CGP049090 in sphere forming assays.

<p>IC₅₀ calculations for the indicated Wnt/β-catenin pathway inhibitors assessed in sphere forming assays with primary tumor and mammary epithelial cells, as well as tumorsphere and mammosphere derived cells.</p

Expression of Wnt pathway genes in tumorspheres (TMS), mammospheres (MMS) and mammospheres induced to differentiate (diffMMS).

<p>A) Heat maps of 3 independent TMS (A, n = 3), MMS (B, n = 3) and diffMMS (C, n = 3) RNA preparations profiled on MOE430A Gene Chips. B–E) qRT-PCR of transcripts encoding components and target genes of the Wnt signaling pathway (* p<0.05, t-test) for all genes shown. F and G) Survival, (*p = 0.005, Log-rank test) and metastasis (*p = 0.0068, Log-rank test), curves for human breast cancer patients classified based on their expression of TMS-related and TMS-unrelated (diffMMS-related) specific Wnt pathway components.</p