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146 Program/Abstract # 441 Regulatory logic of pan-neuronal gene expression in C. elegans Stefanakis, Nikolaos; Carrera, Ines; Hobert, Oliver,Columbia University Biological Sciences, New York, United States The adult C. elegans nervous system consists of 302 neurons grouped in 118 anatomical classes. The morphological and functional diversity of mature differentiated neurons of each class is reflected in their different molecular composition. However, all neurons in a nervous system have common characteristics namely cellular projections and synapses. The molecular correlates to those common features are encoded by pan-neuronal genes. The regulatory programs that govern pan-neuronal gene expression are poorly understood. In this study we have defined a group of genes consisting of synaptic proteins and neuronal-specialized cytoskeleton components that are broadly expressed in the nervous system and we are using promoter bashing analysis and fosmid recombineering technology to address how these genes are transcriptionally regulated. We have found that most of the genes under study are indeed expressed throughout the nervous system of the adult hermaphrodite worm but are also expressed in other tissues. Preliminary analysis on the temporal expression pattern shows that some of these genes are only expressed once postmitotic neurons have been born. In addition, promoter bashing analysis suggests a piecemeal model for the transcriptional regulation of the genes in combination with redundant elements for spatial expression. While there is probably not a common regulatory logic among all genes we investigate the possibility that functionally related genes might be regulated in a common manner. Progress on this analysis will be presented. Program/Abstract # 442 Intercellular calcium signaling in a gap junction-coupled cell network establishes asymmetric neuronal fates in C. elegans Chuang, Chiou-Fen; Schumacher, Jennifer; Hsieh, Yi-Wen; Chang, Chieh, Cincinnati Children's Hospital Research Foundation, Cincinnati, United States The nervous system has an immense variety of neuronal cell types and subtypes that derive from a limited number of progenitors. One general way to diversify neuronal subtypes is to specify different identities and functions of individual cell types through stochastic neuronal fate choices. However, the mechanisms that generate stochastic cellular diversity in the nervous system are only partly understood. The C. elegans left and right AWC olfactory neurons specify asymmetric subtypes, one default AWC OFF and one induced AWC ON , through a stochastic, coordinated cell signaling event. Intercellular communication between AWCs and non-AWC neurons via a NSY-5 gap junction network coordinates AWC asymmetry. However, the nature of intercellular signaling across the network and how individual non-AWC cells in the network influence AWC asymmetry is not known. Here, we demonstrate that intercellular calcium signaling through the NSY-5 gap junction neural network coordinates precise 1AWC ON /1AWC OFF decision. We show that NSY-5 gap junctions in C. elegans cells mediate small molecule passage. We expressed vertebrate calcium buffer proteins in groups of cells in the network to reduce intracellular calcium levels, thereby disrupting intercellular communication. We find that calcium in non-AWC cells of the network promotes AWC ON fate, in contrast to the autonomous role of calcium in AWC to promote AWC OFF fate. In addition, calcium in specific non-AWC promotes AWC ON side biases through NSY-5 gap junctions. Our results suggest a novel model in which calcium has dual roles within the NSY-5 network, autonomously promoting AWC OFF , and non-autonomously promoting AWC ON . Program/Abstract # 443 Voltage- and calcium-activated BK potassium channels establish left-right neuronal asymmetry in C. elegans Schumacher Tucker, Jennifer, Cincinnati Children's Hospital Research Foundation, Cincinnati, United States; Chang, Chieh; Chuang, Chiou-Fen (Cincinnati Children's Hospital Research Foundation, Cincinnati, OH, United States) Many highly specialized cells must derive from a limited number of progenitors during nervous system development. An example of neuronal diversification is establishment of asymmetric gene expression across the left-right (L-R) axis, which occurs in the C. elegans AWC olfactory neuron pair. Expression of the odorant receptor str-2 in AWC is random: either the right or left AWC expresses str-2 to become AWC ON, and the other cell becomes AWC OFF. The default AWC OFF fate is executed by a Ca 2+ -regulated kinase cascade that is activated by influx of Ca 2+ through the voltage-gated Ca 2+ channel UNC-2/UNC-36. Intercellular communication between the AWCs and other neurons through the NSY-5/innexin gap junction network induces AWC ON fate. nsy-5 may antagonize the Ca 2+ kinase cascade by inhibiting unc-2/unc-36 activity, but how signals from gap junctions are transmitted to Ca 2+ channels is unknown. Changes in membrane potential can be propagated by gap junctions, and voltage affects L-R asymmetry in Xenopus embryos. To determine if voltage plays a role in establishing AWC asymmetry, we investigated the role of the voltage-and Ca 2+ -activated BK potassium channels in AWC asymmetry. BK channels are outward-rectifying ion channels that play major roles in neurotransmission, but little is known about their role in cell fate determination. We find that two BK channels redundantly promote AWC ON
147 fate, potentially acting downstream of nsy-5 to antagonize Ca 2+ channel activity by decreasing voltage across the membrane. These results establish a novel role for BK channels in neuronal fate diversification. Program/Abstract # 444 Sox genes in C. elegans: sox-2 role in postembryonic development Vidal Iglesias, Berta; Hobert, Oliver, Columbia University Medical Center, New York, United States Sox proteins are a highly conserved family of transcription factors involved in several developmental processes. Expression of SoxB genes correlates with the commitment of cells to a neural fate; however, the relevance of SoxB proteins in early vertebrate neurogenesis has been difficult to prove genetically due to embryonic lethality and presumed redundant functions. The nematode C. elegans has only 5 sox genes: sox-2 and sox-3 form the SoxB group while sem-2, sox-4 and egl-13 belong to other Sox groups. Our results show that sox-2 and sem-2 are the sox genes expressed earliest and in a broader manner during embryogenesis, being expressed in several neuronal progenitors. sox-3, sox-4 and egl-13 are expressed in few cells during late embryogenesis, when most neurons are already born. Both sox-2 and sem-2 null mutants are early larval lethal but do not show neuronal specification defects during embryonic development as indicated by quantification of a panneuronal reporter. Potential redundancy or compensatory mechanisms between different sox genes have been ruled out, strongly suggesting that sox genes are not required for specification of embryonically-derived neurons. However, at the first larval stage there are still several blast cells that will give rise to different postembryonic lineages, which generate several neurons amongst other cell types. Interestingly, sox-2 is expressed in many of these progenitor cells. Using mosaic analysis we have so far identified neurons derived from two different postembryonic lineages which fail to be generated in C. elegans sox-2 mutants. These results support the idea that postembryonic progenitor competence is compromised in the absence of sox-2. Program/Abstract # 445 The induction of pluripotent mesoderm from axolotl animal caps by Brachyury and BMP-4 Ferjentsik, Zoltan; Chatfield, Jodie; Johnson, Andrew, University of Nottingham School of Biology, Nottingham, United Kingdom We developed axolotl embryos as a model system to investigate the development of primordial germ cells (PGCs) from pluripotent cells. Axolotls are a model for the tetrapod ancestor and so accurately represent the amphibian ancestor to mammals. As such, they share the gene regulatory networks (GRN) that control mammalian development, including the GRN for pluripotency. In normal development axolotl PGCs develop in a posterior mesodermal compartment that acts as a germ cell niche. Importantly, this tissue is not conserved in Xenopus or zebrafish embryos, and so little is known about how it is specified. We showed that forced expression of Brachyury and BMP-4 induces pluripotent mesodermal tissue that will give rise to neural tissue, including a neural tube, in addition to PGCs, and other mesodermal cell types. In normal development this domain is induced by FGF and BMP signalling, in the absence of Nodal signals. We refer to it as pluripotent mesoderm, which is distinct from the typical somatic mesoderm that is induced by Nodal, and we postulate that it is homologous to the posterior mesoderm compartment that is responsible for axial elongation in mice. Discrimination between pluripotent mesoderm and somatic mesoderm is governed by Nanog activity, and it represents one of the earliest cell fate decisions in vertebrate embryogenesis. We are using differential transcriptomics to identify the GRN that governs development of this novel mesodermal tissue, and we are working to understand how FGF signalling interacts with Nanog to control its development. Program/Abstract # 446 FGF signaling is required for lineage restriction but not onset of primitive endoderm program in the mouse blastocyst Kang, Minjung; Artus, Jerome; Piliszek, Ania; Hadjantonakis, Anna-Katerina, Sloan-Kettering Institute, New York, United States Emergence of pluripotent epiblast (EPI) and primitive endoderm (PrE) lineages within the inner cell mass (ICM) of the mouse blastocyst occurs in several steps involving initial co-expression of lineage-specific markers, subsequent mutuallyexclusive marker expression and salt-and-pepper distribution of lineage-biased cells, and sorting of lineage-committed cells into respective layers. Precisely how EPI and PrE lineage commitment occurs is not entirely clear, however FGF/ERK signaling appears to be required. To gain insight into the role of FGF signaling we investigated the phenotype resulting from zygotic and maternal/zygotic Fgf4. Fgf4 heterozygous blastocysts exhibited increased numbers of EPI cells and reduced numbers of PrE cells suggesting that FGF signaling must be tightly regulated to ensure appropriate cell numbers for each lineage. Fgf4 mutants lacked PrE entirely; their ICM comprised exclusively NANOG-expressing cells. Notably, co-expression of EPI and PrE marker was initially established, even in the absence of FGF4. Thus, Fgf4 mutant
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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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Abstracts - Society for Developmental Biology

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