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152 Program/Abstract # 459 Identifying the critical amino acids of SOBP that mediate interaction with the transcriptional regulator Sine oculis Kenyon, Kristy L.; Monaco, Brian, Hobart and William Smith Colleges, Geneva, United States; Moody, Sally (George Washington University, Washington, United States); Pignoni, Francesca (Syracuse, NY, United States); Stout, Josephine (Hobart and William Smith Colleges, Geneva, United States) In Drosophila, Sine oculis binding partner (SOBP) is a novel protein that has been shown to interact with Sine oculis (SO) both in vivo and in vitro (Giot et al., 2003; Kenyon et al., 2005). While the exact function of SOBP remains unknown, both SO and SOBP are co-expressed in the eye-antennal imaginal disc, posterior to the morphogenetic furrow. Taken together, these data suggest that the interaction between the two proteins may have functional consequences for the development of the fly visual system. In this study, we identified a specific subset of amino acids within SOBP that appear to facilitate its interaction with the Six type protein interaction domain of Sine oculis. Based on this determination, the known expression patterns of SOBP, and inherent characteristics of the SOBP protein, we propose several potential functions for the SO/SOBP complex within the developing Drosophila eye. In addition, we tested Xenopus homologues of each factor in the yeast system; initial results indicated that these interactions are conserved in frogs. This research may have relevant implications for mammalian development given the conserved nature of SOBP across phyla. Program/Abstract # 460 A role for Casz1, a homolog of the Drosophila fate determination gene Castor, in murine retinal development. Mattar, Pierre, IRCM, Montréal, Canada; Blackshaw, Seth (Johns Hopkins University School of Medicine, Baltimore, United States); Cayouette, Michel (IRCM, Montréal, Canada) Background: During neural development, different types of neurons and glia are often generated in stereotyped sequences. For example, in the embryonic murine retina, retinal ganglion, horizontal, and amacrine neurons, as well as cone photoreceptors are generated first. Postnatally, progenitors then generate rod photoreceptors, bipolar neurons, and Müller glia. The temporal control of progenitor competence is best understood in Drosophila, where a cascade of transcription factors progressively controls daughter cell identity. This cascade includes the zinc-finger transcription factor Castor. A single orthologous gene, Casz1, is conserved in vertebrate genomes. Here, we elucidate the function of Casz1 in murine retinal development. Results: Casz1 mRNA and protein begins to be expressed in retinal progenitors prior to birth. Casz1 becomes strongly expressed in photoreceptors and some bipolar cells postmitotically. Progenitors transduced with Casz1- expressing retroviruses generate clones that exhibit similar size versus controls, suggesting that Casz1 does not significantly alter progenitor cell cycle parameters or cell death. However, Casz1 misexpression skews the cell-type composition of the resultant clones. When Casz1 is misexpressed in early-stage retinal progenitors, late-born photoreceptors and bipolar cells are disproportionately generated at the expense of early cell types and Müller glia. In accordance with gain-of-function experiments, RNAi-mediated knockdown favors Müller glia at the expense of photoreceptors and bipolar cells. Conclusions: Casz1 may control the competence of retinal progenitors to generate lateborn neuronal types in a manner analogous to the temporal fate determinant Castor in Drosophila. Program/Abstract # 461 Distinct lineage-specific roles for GLI3R mediated control of ureteric induction, branching morphogenesis, and urinary tract patterning. Blake, Josh, University of Toronto, Toronto, Canada; Rosenblum, Norman (SickKids, Toronto, ON, Canada) The transcription factor GLI3 is proteolytically cleaved to a transcriptional repressor (GLI3R) in the absence of Hedgehog signaling (HH). Loss of Sonic Hedgehog ligand in the developing mouse embryo causes renal agenesis or a single ectopic hypodysplastic kidney and implicates GLI3R as a negative regulator of urinary tract formation. Yet specific events perturbed by GLI3R remain undefined. Gli3 Δ699/Δ699 obligately express GLI3R and demonstrate marked renal hypoplasia (100%) and a double collecting system (~47%) at E15.5 (n=12) with hydronephrosis at E18.5 (100%, n=16). Renal hypoplasia is preceded by ureteric bud (UB) hypoplasia at E10.5 & E11.5 and reduced UB branching at E12.5 (51%, n=16). Double collecting systems arise from two primary UBs (67%, n=6) in E11.5 Hoxb7-cre; Rosa lacZ/+ ; Gli3 Δ699/Δ699 mice. Cranial Wolffian duct to bud-site lengths indicated normal positioning of one UB with cranial ectopic positioning of the second (p=0.0026). All UBs failed to maintain position caudally with the CND at E11.5 (p=0.004) and were associated with blind-ended ureters at E16.5 (100%, n=6). UB specific expression of GLI3R in E15.5 Hoxb7-cre;Gli3 TFlag embryos caused renal hypoplasia (100%, n=14) without duplex collecting system. Moreover, mesenchyme specific expression of GLI3R in E15.5 Pax3-cre;Gli3 TFlag embryos caused renal agenesis. Our data demonstrate that GLI3R acts in the ureteric lineage to control bud size and branching morphogenesis and in non-ureteric lineages to control ectopic budding and
153 ureteric insertion into the bladder. Furthermore, mesenchyme-specific expression of GLI3R controls UB induction. Our findings identify multiple and distinct lineage-specific roles for GLI3R in early urinary tract development. Program/Abstract # 462 Stromal signals regulate differentiation of the kidney progenitor population. Carroll, Thomas J., UT Southwestern Med Ctr Internal Medicine and Molecular Biology, Dallas, United States Kidney development in mammals requires reciprocal interactions between the ureteric bud and the adjacent metanephric mesenchyme. Signals from the mesenchyme promote branching morphogenesis of the bud epithelium, while reciprocal signals from this bud epithelium are necessary for the survival and renewal of a progenitor population within the mesenchyme. A signal(s) from the bud also induces a sub-population of the progenitors to undergo a mesenchymal-toepithelial transition (MET) and differentiate into epithelia that will give rise to the kidney nephrons. We identified Wnt9b as signal that is necessary for both progenitor renewal and differentiation. Here, we address the mechanism whereby the same molecule induces two seemingly contradictory processes. We show that signals from overlying stromal fibroblasts modify the progenitor cells’ response to Wnt9b, determining whether they will proliferate or differentiate. This stromal signal is mediated, at least in part, by the atypical cadherin Fat4. Utilizing these two opposing signals, differentiation and growth of nephron progenitors is balanced, assuring proper organ size and function. Program/Abstract # 463 ß-catenin controls branching morphogenesis via the Gdnf Ret Signaling axis during kidney development Sarin, Sanjay, Hamilton, Canada; Li, Aihua; Bridgewater, Darren (Hamilton, Canada) During kidney development, branching morphogenesis gives rise to the collecting duct system through growth, elongation and branching of the ureteric epithelium. The ureteric epithelial induces the metanephric mesenchyme (MM) to undergo nephrogenesis, the formation of nephrons. A failure in these two embryonic processes leads to renal dysplasia, the major cause of childhood renal failure. β-catenin is normally expressed in the MM and over-expressed in renal dysplasia suggesting an important role in kidney development. We generated a mouse model with β-catenin deficiency exclusively in the metanephric mesenchyme. Mutants demonstrated renal hypoplasia by E13.5 and reduced ureteric branching. In-situ hybridization of E11.5 kidneys revealed a marked reduction in Gdnf expression, but no changes in Ret or Wnt11, molecules required for ureteric branching. To support β-catenin controls branching morphogenesis via regulating Gdnf expression we generated a model of β-catenin over-expression exclusively in the metanephric mesenchyme. Mutants displayed severe renal dysplasia and the formation of 4-6 ectopic kidneys. Analysis revealed marked abnormalities in ureteric budding and branching. In situ hybridization of E11.5 kidneys demonstrated increased Gdnf, Ret and Wnt11 expression. A ChIP assay revealed that β-catenin directly bound to a TCF consensus binding site in the Gdnf 5’ untranslated region. Molecular cloning of this 4.9kb fragment upstream of a luciferase gene revealed β-catenin regulates gene transcription from this site. Taken together, these data establish that β-catenin has an essential role in the metanephric messenchyme to guide ureteric budding and branching through the regulation of the Gdnf signaling axis. Program/Abstract # 464 Integrin-linked kinase (ILK) controls ureteric bud (UB) gene expression via p38MAPK-dependent and - independent mechanisms Smeeton, Joanna M.; Rosenblum, Norman, SickKids Toronto, Canada In mammals, the renal collecting system is derived via growth, branching, and remodeling of the UB, a process termed renal branching morphogenesis (RBM). The intracellular signaling pathways that control RBM are largely undefined. Previously, we demonstrated that ILK controls UB branching via p38MAPK in vitro and is required for RBM in vivo (Leung-Hagestejn et al, Mol Cell Biol, 2005; Smeeton et al, Development, 2010). To identify genetic targets of Ilk that regulate RBM, we used whole transcriptome analysis of E12.5 kidneys from mutant mice with Ilk-deficiency in the UB and from controls. Microarray analysis identified 227 differentially expressed mRNA transcripts (p
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1 Program/Abstract # 1 Role of the
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3 Program/Abstract # 7 Forward gene
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5 Program/Abstract # 13 Evolution a
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7 Program/Abstract # 19 Lethal gian
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9 Program/Abstract # 26 On the comb
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11 Program/Abstract # 32 Imaging in
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13 and electron microscopy studies
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15 paracellular space, and interact
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17 the proximal to distal axis of t
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19 Dominguez-Castellano, Maria; Gar
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21 We are interested in the role of
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23 more likely than students who di
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25 was a significant loss of cells
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27 Fgfr3 expression in the limb cho
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29 division, but rapidly loses its
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31 and migration (ADAM13). They act
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33 Program/Abstract # 101 The influ
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35 Program/Abstract # 107 Shroom3-d
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37 Program/Abstract # 113 Requireme
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39 (Queens College, Flushing, Unite
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41 these data imply that Dynamin is
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43 Congenital renal malformations a
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45 Elevated nuclear translocation o
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47 progenitor cells that cover the
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49 abnormally dilated capillaries i
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51 malformations in murine limb bud
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53 Yuqing (Mouse Imaging Centre, To
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55 in the villi at E14. At E11, the
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57 Program/Abstract # 173 The role
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59 Boldt, Clayton, UT Southwestern,
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61 examine stem cell-based CNS rege
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63 Incubation of regenerating cells
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65 learn which dynamic behaviors oc
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67 cell proliferation and for norma
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69 Program/Abstract # 209 Drosophil
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71 cranial neural crest cells, as t
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73 experimental analysis. The jerbo
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75 The through-gut, consisting of s
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77 thereby increasing the chance of
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79 into the role snx5 playsin the N
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81 Lee, Hu-Hui, National Chiayi ers
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83 understood. Here, we have establ
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85 assays, chromatin immunoprecipit
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87 approach. A similar strategy was
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89 verify the functional specificit
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91 Program/Abstract # 278 Heterogen
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93 Program/Abstract # 284 Investiga
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95 Program/Abstract # 290 A molecul
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97 dizygotic twin studies have show
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99 Program/Abstract # 301 Dual role
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Abstracts - Society for Developmental Biology

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