Can pre-implantation biopsies predict renal allograft function in paediatric renal transplant recipients ?

<p>The upper allele was brought by the mother. The number of females with ectopic veins among flies transheterozygous for <i>Elo</i> and <i>corto</i> mutations was compared to the number of females with ectopic veins among flies with a <i>corto</i> mutation only (z-test, ^a p<0.001).</p

<i>Elo</i> genes control wing cell identity.

<p>(A): Wing from control <i>w¹¹¹⁸</i> fly (L1-L5: longitudinal veins; ACV and PCV: anterior and posterior cross-veins). (B, C): Wings from <i>+/EloB^EP3132</i> and <i>EloB^EP3132/Df(3R)BSC518</i> flies exhibit truncated L5. (D): Wings from <i>+/sd::Gal4</i> flies have a very faint ectopic vein phenotype and no margin phenotype. (E, F): Wings from flies over-expressing <i>EloA</i> exhibit ectopic vein and margin phenotypes. (G, H, I): <i>EloC^SH1520</i> and <i>EloC^SH1299</i> loss-of-function alleles diminish expressivity of the ectopic vein phenotype induced by the <i>bs^EY23316</i> loss-of-function allele. Strong phenotype: ectopic veins everywhere in the wing (shown in G). Mild phenotype: ectopic veins under the posterior cross-vein only (shown in H).</p

Decreasing <i>EloC</i> expression suppresses ectopic veins induced by <i>blistered</i> loss-of-function.

<p>The upper allele was brought by the mother. The number of <i>EloC</i>/<i>bs^EY23316</i> females with ectopic veins was compared to the number of <i>+/bs^EY23316</i> females with ectopic veins (z-test, ^a p<0.001). The mild ectopic vein phenotype corresponds to presence of ectopic veins distal to the posterior cross-vein (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0077592#pone-0077592-g005" target="_blank">Figure 5H</a>), whereas the strong ectopic vein phenotype corresponds to presence of ectopic veins everywhere in the wing (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0077592#pone-0077592-g005" target="_blank">Figure 5G</a>).</p

Down-regulation of <i>EloC</i> by RNA interference impairs both cell proliferation and cell differentiation in wing imaginal discs.

<p>(A): Clones expressing the <i>ValEloC</i> transgene (GFP⁺ cells, shown by white arrows) are located at the periphery of the disc and are very small compared to control clones. (B, C, D): Wings from pharates in which <i>ValEloC</i> is driven by <i>nub::Gal4</i> (C) or <i>rn::Gal4</i> (D), both expressed in the wing pouch <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0077592#pone.0077592-StPierre1" target="_blank">[66]</a>, <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0077592#pone.0077592-Ng1" target="_blank">[67]</a> are small compared to wild-type pharate wings (B) and exhibit severe wing blade defects. By contrast, longitudinal veins (shown by asterisks) are formed in the proximal-most part of the wing blade where <i>nub::Gal4</i> and <i>rn::Gal4</i> are not expressed.</p

<i>corto</i> and several TrxG genes control wing cell identity.

<p>(A, B): Ectopic vein phenotypes induced by the <i>corto⁰⁷¹²⁸</i> loss-of-function allele (A) or by <i>corto⁴²⁰</i> loss-of-function clones (B). (C): <i>corto⁴²⁰</i> homozygous clones (GFP^- cells) in wing imaginal discs. (D, E, F): Ectopic vein phenotypes induced by <i>mor</i>, <i>kis</i> or <i>trx</i> loss-of-function alleles. In A, B, D, E, F, asterisks mark ectopic veins.</p

Deregulation of <i>EloA, EloB</i> or <i>EloC</i> expression using <i>P</i>-element insertion lines.

<p>(A): Structure of <i>EloA</i>, <i>EloB</i> and <i>EloC</i> genes showing localization of the <i>P</i>-elements used in this study. Exons are represented by boxes, and introns by lines. Black arrowheads show positions of primer pairs used to quantify <i>Elo</i> gene expression. (B): Quantification of <i>Elo</i> gene expression in <i>EloA^G4930</i>, <i>EloB^EP3132</i>, <i>EloC^SH1520</i> or <i>EloC^SH1299</i> homozygous or heterozygous larvae. (C): Quantification of <i>Elo</i> gene expression in <i>da::Gal4>>EloA^G4930</i> or <i>da::Gal4>>EloB^EP3132</i> larvae. (D): Quantification of <i>EloC</i> expression in <i>da::Gal4</i>>><i>ValEloC</i> embryos. Relative <i>Elo</i> expression levels were obtained by normalization to <i>Rp49</i> (black bars, B to D), <i>RpL12</i> (grey bars, B, C) or <i>eIF-2α</i> (grey bars, D).</p

EloC and Corto bind <i>rho</i> in wing imaginal discs.

<p>(A, B): Wing phenotypes induced by <i>rho</i> loss-of-function (A) or over-expression (B). Asterisks mark truncated L5 (in A) or ectopic veins (in B). (C): Schematic structure of <i>rho</i> with exons represented by boxes and introns by lines. Black arrows show primer pairs used for ChIP experiments. (D): Binding of Corto chromodomain (FH-CortoCD) and EloC (FH-EloC) on <i>rho</i>. For each genotype, the mean of two independent experiments is shown. Error bars correspond to standard deviations.</p