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112 Program/Abstract # 338 Vacuolar Type (H)-ATPase in zebrafish left-right asymmetric development Gokey, Jason; Amack, Jeffrey, SUNY Upstate Medical University, Syracuse, United States Left-right (LR) asymmetry is an interesting and complex aspect of the vertebrate body plan. The Vacuolar Type ATPase, or V-ATPase, is a multi-subunit proton pump that maintains organelle and cellular pH by pumping protons into the organelle lumen and out of the cellular cytoplasm. Small molecule screens have implicated the V-ATPase in vertebrate LR development, however the underlying mechanisms remain unclear. We are using zebrafish to characterize the role(s) of the V-ATPase during LR development. To interfere with V-ATPase function, we treated zebrafish embryos with a small molecule inhibitor of the V-ATPase, concanamycin, or antisense morpholinos that reduce expression of aspecific V- ATPase subunit or an accessory protein. Each of these treatments caused LR patterning defects, such as heart looping defects, and disrupted formation of Kupffer’s vesicle (KV). Motile cilia that project into the lumenof KV generate an asymmetric fluid flow that is required for normal LR development. Interfering with V-ATPase activity significantly decreased the length and number of these cilia and reduced the size of the KV lumen. KVdefects in morpholino-depleted embryos were corrected by ectopic expression of V-ATPase components. Interestingly, over-expression of a V-ATPase accessory protein also disrupted KV, suggesting tight control of V-ATPase activity is critical for normal KV formation. These results indicate V-ATPase function regulates KV formation, a critical step in LR development. Next, we will elucidate mechanisms by which the V-ATPase regulates KV development and embryo LR asymmetry by examining potential connections between V-ATPase activity and the Notch, FGF and Wnt signaling pathways. Program/Abstract # 339 The role of the adherens junction protein aN-catenin in cranial ganglia formation Hooper, Rachel; Taneyhill, Lisa, University of Maryland, College Park, United States Neural crest cells are atransient, multipotent cell population that arises during neurulation and are crucial to normal vertebrate development. After undergoing anepithelial-to-mesenchymal transition (EMT), these cells migrate to their final destinations in the developing embryo and differentiate into a variety ofstructures throughout the adult body. Importantly, improper neural crest cell development has been implicated in human congenital and hereditary malformations, diseases and cancers, thus making the study of neural crest cells absolutely vital. We have previously shown that αN-catenin, a neuralsubtype of an adherens junction protein that is expressed later in many non-neural crest neuronal derivatives, plays an important role in controllingneural crest cell EMT and migration. Although down-regulation of αN-catenin is critical for initial stages of neural crest cell migration, the potential functional role of αN-catenin in later neural crest cell migration and differentiation is not known. To address this question, we investigated the spatio-temporal distribution of αN-catenin at later stages of chick development and examined effects on neural crest cell movement and contribution to cranial ganglia after αN-catenin perturbation.Our data reveal that αN-catenin is re-expressed by migratory cranial neural crest cells contributing to the trigeminal ganglia. Over expression or knockdown of αN-catenin reduces or expands the migratory neural crest cell domain, respectively, leading to a disruption in trigeminal ganglia formation that may be partially due to effects on placode cells. Collectively, our results revealan important later function for αN-catenin in cranial neural crest cell migration and differentiation. Program/Abstract # 340 FOXA2 regulates cell behaviors to induce median hinge point in the neural plate Amarnath, Smita; Bayly, Roy; Eom, Dae Seok; Agarwala, Seema, University of Texas at Austin, United States During neural tube closure, dynamic cell behaviors at specialized regions (hinge points/HP) of the neural plate help fold it into a neural tube. The molecular mechanisms regulating HP formation are poorly understood. We have demonstrated that spatial and cell-cycle dependent temporal modulation of BMP signaling regulates median HP (MHP) formation by interacting with the apicobasal polarity pathway. These interactions stabilize epithelial organization, and thuscyclic BMP attenuation alters neuronal apicobasal polarity sufficiently to give the neural plate the flexibility to roll up and close into a neural tube. However, the question of how the BMP signal itself is dynamically modulated remains unanswered. In this study, we have used in vivo gene misexpression, high-resolution imaging and biochemical analyses to identify the winged helix transcription factor FOXA2 as a potential modulator of both BMP signaling and the apicobasal polarity pathway. In addition, we demonstrate that FOXA2 biochemically interacts with another subfamily (TGFß/Nodal) of Transforming Growth Factor ß ligands, known to regulate cell polarity during epithelial to mesenchymal transformation. Interestingly, increased TGFß signaling in the midbrain mimics the effects of canonical BMP blockade and FOXA2 misexpression, and is sufficient to induce MHP formation. We propose that FOXA2 regulates apicobasal cell polarity and MHP formation by dynamically regulating cross-talk between BMP and TGF-β/Nodal signals cascades.
113 Program/Abstract # 341 Coordination between canonical and non-canonical Wnt signaling patterns the neuroectoderm along the anteriorposterior axis of the sea urchin embryo Range, Ryan; Angerer, Robert; Angerer, Lynne, National Institutes of Health NIDCR, Bethesda, United States The mechanisms that specify and pattern the neuroectoderm along the anterior-posterior (AP) axis regulate one of the most important events to occur during the early development of deuterostome embryos. However, these mechanisms are incompletely understood. The anterior neuroectoderm (ANE) of the deuterostome sea urchin embryo has regulatory properties and factors that are remarkably similar to those in the early vertebrate ANE (forebrain/eyefield), which is initially patterned along the AP axis by Wnt signaling. We tested the functions of several Wnt pathway members and our results show the early sea urchin embryo integrates information from several different signaling pathways to pattern the neuroectoderm, including the Wnt/β-catenin, Wnt/Fzl5/8-JNK, Fzl1/2/7 and PKC pathways. Together, through the Wnt1 and Wnt8 ligands, these pathways provide precise spatio-temporal control of aposterior-to-anterior wave of respecification that restricts the initial, ubiquitous, maternally specified ANE regulatory state to the most anterior blastomeres. Moreover, we show that the Wnt receptor antagonist, Dkk1, protects the ANE fate of these cells through a negative feedback mechanism during the later stages of ANE patterning. Our data indicate that these Wnt pathways converge on the same cell fate specification process, suggesting they function as integrated components of a Wnt signaling network. Our findings also provide strong support for the idea that the sea urchin ANE regulatory state and the patterning mechanisms that position and define its borders were present in the common echinoderm/vertebrate ancestor and still operate to specify anterior neural identity in deuterostome embryos. Program/Abstract # 343 Multiple Wnt signaling phenotypes in Porcupine homolog mutant mouse embryos Biechele, Steffen, Sickkids Research Institute, Toronto, Canada; Cox, Brian J. (University of Toronto, Department of Physiology, Toronto, Canada); Lanner, Fredrik; Rossant, Janet (The Hospital for Sick Children Research Institute, Toronto, Canada) In mammals, the X-chromosomal Porcupine homolog (Porcn) gene is required for the acylation and secretion/function of all Wnt ligands tested to date. Porcn thus represents a bottleneck in the secretion of all 19 mammalian Wnt ligands. We have generated a mouse line carrying a floxed allele for Porcn as a tool to ablate Wnt sources and investigated embryonic requirements for Wnt ligands. Zygotic Porcn mutants fail to gastrulate and phenocopy Wnt3 mutants, indicating a key role for zygotic Wnts in initiating gastrulation. Similarly, maternal-zygotic Porcn mutants display no defects prior to gastrulation, questioning the relevance of Wnt signaling in pre-implantation development. Heterozygous female embryos exhibit parent-of-origin-specific phenotypes due to imprinted X chromosome inactivation in extra-embryonic tissues; maternal allele mutants display chorio-allantoic fusion defects consistent with Wnt7b mutants. In contrast, paternal allele deletion leads to lethality between E11.5 and P3. Rare surviving females present with skin, hair growth and bone defects, similar to human Focal DermalHypoplasia (FDH) patients carrying mutations in PORCN. In summary, we have generated a tool to ablate Wnt ligand secretion, allowing the identification of Wnt sources and functional redundancy of Wnt ligands in the mouse. Based on our studies, Porcn is required for gastrulation, but not during pre-implantation development. Further, Porcn heterozygous females recapitulate phenotypes of Wnt7b and human PORCN mutations, depending on which allele is affected. The Porcn floxed allele will allow for a better understanding of Wnt post-translational modification as well as ligand redundancy in development and disease. Program/Abstract # 344 Retinoic acid is required for head development and is involved in syndromes with craniofacial malformations Gur, Michal, The Hebrew University of Jerusalem, Jerusalem, Israel; Pillemer, Graciela (Jerusalem, Israel); Niehrs, Christof (Hidelberg, Germany); Fainsod, Abraham (Jerusalem, Israel) Retinoic acid is a central signaling molecule regulating several important processes during early embryogenesis. This same molecule is also known to have teratogenic effects on head development when abnormally expressed. Despite this negative role on head formation, several syndromes exhibiting craniofacial malformations, such as DiGeorge/Velocardiofacial, Vitamin A Deficiency and Fetal Alcohol syndromes, suggest a requirement for retinoic acid for normal head development. In order to study the role of retinoic acid in head formation we used the frog Xenopus laevis as a model system, which allowed us to focus on early events inhead formation while manipulating retinoic acid levels. Inhibition of retinoic acid biosynthesis in Wnt8-induced secondary axes resulted in a significant reduction of head formation. By manipulating retinoic acid levels at different developmental stages and different regions of the embryo, we were able to map the requirement for retinoic acid to early gastrula stages, corresponding to the activity of retinoicacid in the Spemann’s organizer. Treatment with high doses of retinoic acid signaling inhibitors resulted in severe gastrulation defects. Lower
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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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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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Page 69 and 70: 69 Program/Abstract # 209 Drosophil
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Page 91 and 92: 91 Program/Abstract # 278 Heterogen
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Page 99 and 100: 99 Program/Abstract # 301 Dual role
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Page 151 and 152: 151 Program/Abstract # 456 Thoracic
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Abstracts - Society for Developmental Biology

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