Abstracts - Society for Developmental Biology

More documents

Recommendations

Info

120 Program/Abstract # 362 Characterizing M9.17, a strong dominant enhancer of the trio and abl mutant phenotypes Liebl, Eric C.; Dean, Katie; Fields, April; Geer, Marcus; King, Eric; Lynch, Brian; Palozola, Katie; Steenkiste, Elizabeth; Zhang, Yan, Denison University, Granville, United States We explore signaling networks involving the trioguanine-nucleotide-exchange factor using second site modifier genetics. Trio is expressed in axonal growth cones, and so we hope to further define networks controlling targeted axon outgrowth. M9.17 is a mutation isolated as a strong dominant enhancer of the trio mutantphenotype. We have found M9.17 also functions as a strong dominant enhancer of the abl mutant phenotype, which is significant as abl is also highly enriched in growth cones. M9.17 was generated by gamma-ray mutagenesis and was mapped to 64 cM on the second chromosome. Fine mapping, complementation analysis and genomic DNA sequencing have shown that M9.17 is caused by a 23-base pair deletion within the sequoia gene. Sequoia is a zinc-finger transcription factor, originally isolated by its effects on axon and dendrite morphogenesis. This deletion cases a frame-shift resulting in 260 novel residues following sequoia’s Q561. This novel sequoia allele is a neomorph as neither sequoia-null deficiencies nor seq[vr5-5] (Q641STOP) function as dominant enhancers of the trio mutant phenotype. Unexpectedly, M9.17’s enhancement of the trio mutant phenotype is not due to disruptions of early CNS architecture. Rather, these animals survive normally to 3rd-instar larvae, but then fail to pupate. Classic behavioral assays have demonstrated they fail to switch from “forager” to“wanderer” 3rd-instar larvae. Other work on this behavioral switch has implicated the larval mushroom body. Therefore our future work will focus on trying to understand how M9.17’s strong, dosage sensitive genetic interaction with both trio and abl may affect mushroom body neuronal circuitry involved in the forager-to-wanderer behavioral switch. Program/Abstract # 363 TrkB, TRPC3, and Ca2+ regulation of primary afferent extension in the embryonic avian spinal cord McNamara, Michelle A.; Ezerman, Elizabeth; Romaner, Brian; Clason, Todd; Forehand, Cynthia, University of Vermont, Burlington, United States During neural development, dorsal root ganglia (DRG) sensory axons extend into the spinal cord at the dorsal root entry zone (DREZ), then branch to grow longitudinally along the rostral-caudal axis and finally grow into the grey matter. Our laboratory is interested in the regulation of longitudinal growth of sensory axons in the developing spinal cord. Using an in vitro preparation, we have shown that axon extension in the longitudinal pathway is significantly reduced by inhibition of TrkB or BDNF in the St. 25 chicken embryo. While the data suggest a role for TrkB and BDNF in this growth pattern, the mechanism is unknown. BDNF is an activator of a cation current that has been shown to require components of the BDNF induced PLCγ intracellular signaling pathway including phospholipase C, IP3 receptors, release of Ca2+ stores and Ca2+ influx. In addition, transient receptor potential canonical subfamily (TRPC) channels, specifically TRPC3, have been shown to co-localize with TrkB and become activated in a PLCγ dependent manner. Here we show immunoreactivity for TRPC3 in the DRG, DREZ and longitudinal pathway at St. 25. Further, we show that removal of extracellular Ca2+ or application of U7322, an inhibitor of PLCγ, significantly decreases DRG axon extension along the longitudinal axis of the embryo. These data suggest that TRPC3 and the PLCγ signaling pathway may mediate the role of BDNF and TrkB in DRG axon extension in the developing longitudinal pathway. Program/Abstract # 364 Cdc42ep1 facilitates the efficient migration of cranial neural crest cells Nie, Shuyi, Pasadena, United States CDC42 is a small GTPase of the Rho-subfamily, which regulates signaling pathways that control diverse cellular functions including cell morphology, migration, endocytosis and cell cycle progression. We have identified a cdc42 effector protein cdc42ep1 in Xenopus embryos that is predominantly expressed in premigratory and migrating neural crest cells. Depletion of Cdc42ep1 with antisense morpholino oligonucleotides causes cranialneural crest cells to migrate significantly shorter distances, preventing their segregation into distinct migratory streams. At later stages, this results in severe defects in cartilage formation. Analysis of cranial neural crest cells reveals that Cdc42ep1 is required for the formation of filopodial protrusions, and the polarized distribution of Cdc42. Taken together, these results suggest that Cdc42ep1 interacts with Cdc42 in controlling cell polarization and protrusive activities. Selective expression of Cdc42ep1 in neural crest cells thus facilitates efficient migration of this unique cell population. Program/Abstract # 365 Proteolytic processing of cadherins in chick cranial neural crest cells Schiffmacher, Andrew T.; Taneyhill, Lisa, University of Maryland, College Park, College Park, MD, United States
121 Misregulation of molecular pathways controlling the epithelial-to-mesenchymal transition (EMT) underlying cranial neural crest emigration, including adherens junction disassembly, may adversely affect neural crest development and result in craniofacial defects. Cranial neural crest cells undergo EMT en masse to acquire motility, subsequently migrating throughout the head and differentiating into a diverse range of cell types. In chick midbrain premigratory neural crest cells, N-Cadherin (N-Cad) and Cadherin6B (Cad6B) proteins are down regulated prior toEMT, with their turnover coordinated independently of transcriptional repression. We hypothesize that proteolytic processing depletes cadherin levels to facilitate neural crest EMT. We have verified proteolytic cleavage of Cad6B and N-cad in vivo at stages immediately following EMT by immunoblotting of midbrain lysates. To identify the protease(s) responsible for this cleavage, we have co-expressed relevant candidate metalloproteinases observed in the chick midbrain with Cad6B or N-cad in vitro and have identified members of the A Disintegrin and Metalloproteinase (ADAM) family to be important for cadherinc leavage. We will now perform over expression and knock-down assays in vivo to confirm these in vitro results and to assess subsequent effects on cadherin localization and neural crest cell EMT and migration. Collectively, our work will facilitate a better understanding of the molecular mechanisms underscoring normal developmental and disease-related EMTs. Program/Abstract # 366 Regulation of Slit-Robo signaling by Comm-family members in insects Seeger, Mark, Columbus, United States; Carver, Laura; Jowdy, Casey (Columbus, United States) Slit-Robo signaling is a key mediator of axon guidance decisions in divergent organisms ranging from planaria to vertebrates. In Drosophila melanogaster, Commissureless (Comm) is a key post-translational regulator of the Robo receptor and functions to prevent cell surface accumulation of Robo. Two additional Comm-family members are found in Drosophila and they vary in their ability to regulate Robo receptors. Although all three Comm-family members can complex with Robo receptors, only Comm and Comm2 regulate Robo receptor distribution in a Drosophila S2 cell culture assay. In vivo loss-of-function and gain-of-function assays reveal prominent roles for Command minor roles for Comm2 during embryonic development. Structure-function studies suggest that the functional differences amongst Comm-family members map to the trans-membrane and juxta-membrane regions of these proteins. Results from these ongoing studies will be presented. We are also investigating the evolution of Comm-like genes and regulation of Slit-Robo signaling in insects. The presence of Comm-family members in some insect orders (Diptera and Hemiptera) and apparent absence in others (Lepidoptera and Hymenoptera) suggests a more ancient origin of Comm and the loss of Comm-like genes in some but not all insect lineages. We are addressing the functional properties of divergent Comm-family members from a variety of insects using several approaches, including the S2 cell culture assay. This work has been supported by a grant from the National Science Foundation. Program/Abstract # 367 Behavioral phenotypes after selective abrogation of Arx from the developing dorsal telencephalon Simonet, Jacqueline C., University of Pennsylvania Cell and Developmental Biology, Philadelphia, United States; Marsh, Eric; Golden, Jeffrey (Children's Hospital of Philadelphia, Philadelphia, PA, United States) The aristaless-related homeobox gene (Arx) is mutated in many neurodevelopmental disorders all including neurocognitive phenotypes. During development Arx is expressed in progenitor cells throughout the forebrain. In the pallium Arx is expressed in the proliferative ventricular zone (VZ) where the excitatory neurons of the cortex are born. Arx-/y mice have decreased proliferation in the VZ of the cortex resulting in a thinner cortex, however, these mice die soon after birth precluding behavior analyses (Kitamura et al. 2002). Mice that have a point mutation or a poly-alanine track expansion in Arx survive to adulthood and both were found to have learning deficits with the poly-alanine track expansion mice also exhibiting anxiety and hyperactivity (Kitamura et al. 2009). To evaluate how Arx is affecting the development and function of the excitatory neurons of the cortex, we conditionally eliminated Arx selectively from the precursors to all cerebral cortical projection neurons without affecting the interneuron population. These mice lose upper layer neurons resulting in a thinner cortex. The corpus callosum and the anterior commissure are hypoplastic or absent suggesting cortical and possibly amygdala and hippocampal, connectivity are perturbed. Behaviorally these mice are less anxious, more active, less social, and have focused learning deficits when compared to their wild type littermates. Furthermore, compared to all other Arx mutant mice that have been studied, they do not have seizures. This mutant mouse provides an important tool in which to study the function of Arx in brain development and behavior without seizures confounding the analysis. Program/Abstract # 368 A screen to identify interactors of the antiphosphatase Paladin in the neural crest Stronge, Edward J.; Roffers-Agarwal, Julaine; Gammill, Laura S., University of Minnesota, Minnneapolis, United States
Page 1 and 2:
1 Program/Abstract # 1 Role of the
Page 3 and 4:
3 Program/Abstract # 7 Forward gene
Page 5 and 6:
5 Program/Abstract # 13 Evolution a
Page 7 and 8:
7 Program/Abstract # 19 Lethal gian
Page 9 and 10:
9 Program/Abstract # 26 On the comb
Page 11 and 12:
11 Program/Abstract # 32 Imaging in
Page 13 and 14:
13 and electron microscopy studies
Page 15 and 16:
15 paracellular space, and interact
Page 17 and 18:
17 the proximal to distal axis of t
Page 19 and 20:
19 Dominguez-Castellano, Maria; Gar
Page 21 and 22:
21 We are interested in the role of
Page 23 and 24:
23 more likely than students who di
Page 25 and 26:
25 was a significant loss of cells
Page 27 and 28:
27 Fgfr3 expression in the limb cho
Page 29 and 30:
29 division, but rapidly loses its
Page 31 and 32:
31 and migration (ADAM13). They act
Page 33 and 34:
33 Program/Abstract # 101 The influ
Page 35 and 36:
35 Program/Abstract # 107 Shroom3-d
Page 37 and 38:
37 Program/Abstract # 113 Requireme
Page 39 and 40:
39 (Queens College, Flushing, Unite
Page 41 and 42:
41 these data imply that Dynamin is
Page 43 and 44:
43 Congenital renal malformations a
Page 45 and 46:
45 Elevated nuclear translocation o
Page 47 and 48:
47 progenitor cells that cover the
Page 49 and 50:
49 abnormally dilated capillaries i
Page 51 and 52:
51 malformations in murine limb bud
Page 53 and 54:
53 Yuqing (Mouse Imaging Centre, To
Page 55 and 56:
55 in the villi at E14. At E11, the
Page 57 and 58:
57 Program/Abstract # 173 The role
Page 59 and 60:
59 Boldt, Clayton, UT Southwestern,
Page 61 and 62:
61 examine stem cell-based CNS rege
Page 63 and 64:
63 Incubation of regenerating cells
Page 65 and 66:
65 learn which dynamic behaviors oc
Page 67 and 68:
67 cell proliferation and for norma
Page 69 and 70: 69 Program/Abstract # 209 Drosophil
Page 71 and 72: 71 cranial neural crest cells, as t
Page 73 and 74: 73 experimental analysis. The jerbo
Page 75 and 76: 75 The through-gut, consisting of s
Page 77 and 78: 77 thereby increasing the chance of
Page 79 and 80: 79 into the role snx5 playsin the N
Page 81 and 82: 81 Lee, Hu-Hui, National Chiayi ers
Page 83 and 84: 83 understood. Here, we have establ
Page 85 and 86: 85 assays, chromatin immunoprecipit
Page 87 and 88: 87 approach. A similar strategy was
Page 89 and 90: 89 verify the functional specificit
Page 91 and 92: 91 Program/Abstract # 278 Heterogen
Page 93 and 94: 93 Program/Abstract # 284 Investiga
Page 95 and 96: 95 Program/Abstract # 290 A molecul
Page 97 and 98: 97 dizygotic twin studies have show
Page 99 and 100: 99 Program/Abstract # 301 Dual role
Page 101 and 102: 101 trafficking of cargo proteins a
Page 103 and 104: 103 Sonic Hedgehog (Shh) is a secre
Page 105 and 106: 105 tube was aberrant. Our data ind
Page 107 and 108: 107 degradation of Smad proteins. W
Page 109 and 110: 109 strong affects on organogenesis
Page 111 and 112: 111 that maternally-supplied Lkb1 i
Page 113 and 114: 113 Program/Abstract # 341 Coordina
Page 115 and 116: 115 partners. Our transgenic gain o
Page 117 and 118: 117 delayed and stunted as monitore
Page 119: 119 Program/Abstract # 359 The meth
Page 123 and 124: 123 back to the midbody in cbp-1 RN
Page 125 and 126: 125 versus asymmetric cell division
Page 127 and 128: 127 spinal cord. Iulianella, Angelo
Page 129 and 130: 129 determine cell cycle activity i
Page 131 and 132: 131 in expanded Lmx1a/b+ progenitor
Page 133 and 134: 133 ROS levels. Collectively, our r
Page 135 and 136: 135 limbs. Apoptosis was also pertu
Page 137 and 138: 137 Henkels, Julia; Zamir, Evan, Ge
Page 139 and 140: 139 however, and its role in CSF ma
Page 141 and 142: 141 embryonic precursors to form an
Page 143 and 144: 143 with fork retarding Replication
Page 145 and 146: 145 homeodomain (HD) transcription
Page 147 and 148: 147 fate, potentially acting downst
Page 149 and 150: 149 involved in Drosophila ventral
Page 151 and 152: 151 Program/Abstract # 456 Thoracic
Page 153 and 154: 153 ureteric insertion into the bla
Page 155 and 156: 155 of p16, a known cyclin kinase i
Page 157 and 158: 157 rax mutant was recently found i
show all

Abstracts - Society for Developmental Biology

Create successful ePaper yourself

Delete template?

Save as template?