Congress Abstracts - Society for Developmental Biology

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appears not to be directly regulated by endoderm convergence. Furthermore, defects in endoderm convergence induced by a deficiency for S1pr2/Gα 13 signaling impaired both the passive and active modes of myocardial precursor migration. We are currently investigating the mechanisms by which S1pr2/Gα 13 controls both endoderm convergence and myocardial migration. Our study is expected to establish a framework for the interplay between the endoderm and myocardial precursors during heart-tube formation. Program/Abstract # 237 A role for Claudin-10 in left-right axis patterning Collins, Michelle M.; Ryan, Aimee (McGill University, Canada) Asymmetric organ positioning within the limited space of the body cavity is critical for normal physiological function. The origin of this asymmetry is initiated during gastrulation in an evolutionarily conserved molecular cascade. We have identified that a transmembrane tight junction component, Claudin-10, plays a role in directing asymmetric organ positioning in the chick. Claudins are integral components of tight junctions. Within the tight junction, claudins play a critical role in the regulation of the movement of ions and small molecular within the paracellular space. Additionally, claudins link the tight junction to the actin cytoskeleton via interactions within their cytoplasmic tails with adaptor and scaffolding proteins. Here, we report that Claudin-10 mRNA and protein are asymmetrically expressed on the right side of Hensen’s node, a critical site where bilateral symmetry is broken. We demonstrate that overexpression of Claudin-10 on the left side of the node, or knockdown of endogenous Claudin-10 on the right side of the node, randomizes the direction of heart-looping, the earliest morphological sign of disrupted left-right patterning. Furthermore, expression of classic left-right patterning genes Nodal, Lefty, Pitx2c, and cSnR is randomized in manipulated embryos. Mutagenesis of charged residues in the domain determining ion permeability properties did not affect the function of Claudin-10 in asymmetric organogenesis. However, mutation of two sites in the cytoplasmic tail (PDZ-binding domain and a putative phosphorylation site at S218) abolished the ability of Claudin-10 to randomize the direction of heart looping in gain-of-function studies, suggesting that interactions with cytoplasmic proteins are critical for Claudin-10 function. We are currently exploring the mechanism by which Claudin-10 functions in patterning the left-right axis. Program/Abstract # 238 Dynamic cell rearrangement driving early heart tube formation and looping Saijoh, Yukio; Kidokoro, Hinako (University of Utah, USA); Tamura, Koji (Tohoku University, Japan); Okabe, Masataka (The Jikei University School of Medicine, Japan); Schoenwolf, Gary (University of Utah, USA) The vertebrate heart forms by the fusion of the paired left and right fields of precardiac mesoderm, which are originally separated on the either side of the embryonic midline. The short and symmetric primitive heart, undergoes rapid elongation along the A-P axis as the fusion proceeds, transforming from a straight morphology into a C-shaped loop. The asymmetric looping usually orients the heart tube toward the right side of the embryo, and several laterality genes that are expressed exclusively on the left side of the heart field have been shown to control the directionality of the looping. However, the behaviors/properties of cells that are modified by the leftright signals to drive morphogenesis remain unknown. To address this, we first analyzed in detail morphological changes of the heart tube during C-looping and found that C-looping is accomplished by asymmetric tissue growth between the left and right heart rudiments. Using cell labeling with fluorescent dyes and time-lapse microscopy, we further investigated how precardiac tissues are arranged during heart tube formation and C-looping. Our observations suggested that heart precursor cells undergo dynamic rearrangement during these processes to transform the sheet-like structure of the precardiac mesoderm into a single elongated tube and to shape the primitive heart. Detailed analyses comparing movements of groups of labeled cells in the left and right heart primordia revealed that each primordium undergoes different patterns of rearrangement during heart morphogenesis. We will discuss differences in cell properties between left and right heart tissues that control differential tissue rearrangement and tissue growth to drive asymmetric looping. Program/Abstract # 239 Importancia de microRNAS en la embryogénesis del tracto de salida ventricular derecho. Estudio en el embrión de pollo Sanchez Gomez, Concepcion, (Hospital Infantil Federico Gomez, Mexico), Perez, Carmen (UNAM, Mexico) El objetivo fue determinar el patrón de expresión de 13 miRs cardiacos en la región del corazón embrionario de pollo incluyendo al cono, tronco y saco aórtico durante su transformación en tractos de salida y troncos arteriales (St.24-36HH). Se seleccionó 13miRs cardiacos, se disectó la zona de interés y se obtuvo tejido adulto de tractos de salida ventrículares y troncos arteriales. Se extrajo el RNA total por el método de Trizol, se amplificó por RT-PCR. La expresión relativa se calculó con el método ∆CT y se empleo Anova una vía y una prueba post-hoc Tukey p ≤0.005. En St.24HH, la mayoría de los miRs estaban subexpresados respecto a la expresión en estructuras maduras, excepto cuando se comparó con el tracto de salida ventricular derecho. En este caso, el tejido embrionario mostró la mayoría de los miRs sobreexpresados. Por búsqueda bioinformatica y en la literatura, se encontró que miRs 206, 23b, 24 y Let7 están relacionados con TGF- b , importante en la TEM necesaria para el desarrollo de las crestas conales. Estos miRs fueron evaluados de St.24-36HH y se investigo sus blancos. Al comparara tejido embrionario con tracto de salida ventricular derecho se halló que en St. 24HH cuando TEM ya no es importante para el desarrollo de crestas conales, miR206 y 23b están sobreexpresados, después desaparecen. El blanco de miR206 es la endotelina y de miR 23b la acido hialurónico sintetasa, ambos modifican la MEC. miR24 inhibe la síntesis y secreción de TGF- b , que promueve la regulación de TEM. Estos eventos en conjunto provocan descenso de TEM, 68
facilitan cambio en patrón morfogenetico del mesénquima de crestas conales hacia la proliferación y maduración del tejido. Let7 no participa. Program/Abstract # 240 The Cellular Basis of Limb bud Initiation Gros, Jerome, (Institut Pasteur, France), Tabin, Cliff (Harvard Medical School, USA) Vertebrate limbs first emerge as small buds at specific locations along the trunk. While a fair amount is known about the molecular regulation of limb initiation and outgrowth, surprisingly, the cellular events underlying these processes have remained less clear. Here we show that the mesenchymal limb progenitors arise through localized Epithelial-to-Mesenchymal Transition (EMT) of the coelomic epithelium specifically within the presumptive limb fields, and that this process is the initiating event of limb bud formation. This EMT is absolutely necessary to initiate limb buds and is regulated at least in part by Tbx5 and Fgf10 (key players in the molecular circuitry known to genetically control limb initiation). The finding that limb buds initiate earlier than previously anticipated through an EMT event and not through differential proliferation rates, as previously proposed, represents a paradigm shift that changes the way one views the earliest events of limb formation and redefines the question of how the limb buds are placed at the proper axial location. Program/Abstract # 241 Gene regulation that initiates Sonic hedgehog expression in the limb bud Tamura, Koji, (Tohoku University, Japan), Matsubara, Haruka; Yokoyama, Hitoshi (Tohoku University, Japan) Sonic hedgehog (Shh) is a key molecule that plays a central role in limb morphogenesis. Shh expression in the early limb bud begins at a restricted small area of the lateral mesoderm as a very small dot at the posterior margin of the bud. Genetic and embryological evidences in the mouse and chick have suggested that positive regulators, such as dHAND, Hoxd11/d12 and Tbx2/3, and negative regulators, including Gli3R and Alx4 , restrict the domain of Shh expression, determining the position of posterior-localized Shh in early limb bud. However, available data in published reports and our own detailed observations indicate that these genes are expressed in a region larger than the epression domain of Shh, suggesting that the posterior-restricted initiation of Shh expression cannot be completely explained by any combinations of expression of these genes. To overcome this incompleteness, we further focused on Tbx2/3, Hoxd12 and Fgf8 and examined the expression pattern of these genes in detail in sections. Tbx2, an upstream inducer of Shh , is expressed at the posterior (and anterior) periphery of the limb bud mesenchyme, and Tbx2 expression is negatively regulated by Fgf8. Hoxd12, which can induce Shh, is expressed in posterior margin of the limb bud mesenchyme simultaneously Shh. FGFs are known to have a function in maintenance of Shh expression with a feedback loop. Fgf8 is expressed in a special epithelial tissue, the apical ectodermal ridge (AER). We found that Shh expression begins at a small area within Tbx2/3 and Hoxd12 positive domain underneath the posterior margin of Fgf8 expression. These results suggest that the initial position of the Shh expression domain corresponds to the Tbx2/3 and Hoxd12-positive region underneath the Fgf8-positive ectoderm at the posterior edge of the AER. Program/Abstract # 242 Expression and functional analysis of transcription factor AP-2ß in limb development Seki, Ryohei (MRC National Institute for Medical Research, UK); Suzuki, Takayuki (Nagoya University, Japan); Yokoyama, Hitoshi; Tamura, Koji (Graduate School of Life Sciences, Japan) Tetrapods have two pairs of limbs, which exhibit diverse morphology in digits. The length of a digit depends on the number and length of phalanges. To elucidate the mechanisms that regulate these two parameters, we focused on a human familial syndrome called Char syndrome causing digit malformation, including shortness and disappearance of the skeleton. It has been reported that the responsible gene is the transcription factor AP-2β. Thus, we hypothesized that in normal development, AP-2β regulates the length and number of skeletal elements in digits. We first investigated using chick embryos whether AP-2β carrying the same mutation as that in Char syndrome gave rise to skeletal malformation of digits. The resultant limbs showed shortness and disappearance of the skeleton. The expression analysis of AP-2β revealed a good correlation between the digit length and duration of AP-2β expression. Further investigations suggested that AP-2β functions downstream of FGF signals from the apical ectodermal ridge, an epithelial structure essential for limb outgrowth. Gain of function of AP-2β, however, resulted in no alteration in limb skeletal pattern. Co-overexpression of AP-2β with AP-2α, which is another member of the AP-2 family and is also expressed in the distal limb bud, resulted in limb skeletal malformations. To further elucidate the function of AP-2β, we examined alterations in cell proliferation, cell death and expression pattern of some key genes involved in limb outgrowth or morphogenesis when the dominant-negative AP-2β was introduced. Based on the results, we will discuss the mechanism of digit morphogenesis from the viewpoint of AP-2β function. Program/Abstract # 243 Role of transcription factor EVI-1 in chondrogenesis Cela, Petra; Balkova, Simona (Institute of Animal Physiology and Genetics, Czech Republic); Horakova, Dana; Buchtova, Marcela (University of Veterinary and Pharmaceutical Sciences, Czech Republic); Richman, Joy M. (Life Sciences Institute, University of British Columbia, Canada) Ecotropical viral integration site 1 (EVI-1) is a transcription factor essential for vascularisation and cell proliferation during embryogenesis. In our previous experiment, we analysed its expression during chicken embryonic development. Since strong 69
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International Society of Developmen
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neural crest cells (hNCC)) human em
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activity may determine the orientat
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Developmental cell signaling pathwa
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opposed roles during early gastrula
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functions by the recruitment of add
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function validated with explant stu
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Program/Abstract # 48 Modeling regu
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Page 19 and 20: morphologies. Our analyses not only
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Page 23 and 24: Program/Abstract # 78 In vivo recep
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Page 27 and 28: Program/Abstract # 92 The C. elegan
Page 29 and 30: Program/Abstract # 98 A gradient of
Page 31 and 32: Program/Abstract # 106 Developing a
Page 33 and 34: NSCs, but not in neurons, bind not
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Page 45 and 46: Program/Abstract # 156 Systematic I
Page 47 and 48: Program/Abstract # 163 Size regulat
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Page 51 and 52: Penaeid shrimp represent an importa
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Page 61 and 62: condition. Kanyon embryos have a mi
Page 63 and 64: Program/Abstract # 218 Lfng regulat
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Page 89 and 90: Program/Abstract # 308 Mechanistic
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Page 93 and 94: Program/Abstract # 323 Drosophila g
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stem cell‐like characteristics. H
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diminished. Interestingly, we found
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y invading osteoblasts. Quite diffe
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coimmunoprecipitation experiments d
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cells and sub-cellular endosomal co
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accumulation is decreased. This wor
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Sex determination in vertebrates de
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Program/Abstract # 462 Retinaldehyd
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Program/Abstract # 469 Search for n
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growth factors used to keep them al
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it is still required to promote mig
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on the outside of small clear vesic
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Program/Abstract # 497 mef2ca contr
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were colocalized along the epidermi
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neural tube morphogenesis, is conse
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Hypoxia-inducible factors (HIFs) ar
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To address this issue, we have take
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Program/Abstract # 530 The MADS pro
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Better understanding of the underly
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NPCs blunted proliferation in the S
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Program/Abstract # 551 Evolutionari
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group is interested in inferring an
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Program/Abstract # 564 Withdrawn Pr
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Program/Abstract # 573 Fluoride ind
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oligodendrocytes of the central ner
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cycle, no changes were observed in
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have begun to document the targets
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Congress Abstracts - Society for Developmental Biology

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