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26 and acts at a step that is dependent on the extracellular domain of Notch. Our results are consistent with the possibility that Uif regulates the accessibility of the Notch extracellular domain to its ligands during Notch activation. Our study thus identifies a new modulator that can fine tune Notch activity, further illustrating the importance of a delicate regulation of this signaling pathway for normal patterning. Program/Abstract # 80 Tenascin is a correlative marker in uterine fibroid Choi, YunJeong; Park, HyoSang; Lee, Seulkina; Park, YoungHoon; Kang, Sua; Kim, DaeYoung; Hwang, YouJin (Gachon University of Medicine and Science, Incheon, Republic of Korea) Uterine fibroids are the most common benign tumors in the female reproductive system. However, the contributing factors to the growth of fibroids are hardly known, and there are only few effective methods to treat uterine fibroid. The extracelluar martrix (ECM) plays a fundamental roles in the regulation of diverse cellular events. Tenascin is an ECM glycoprotein and it takes part in cell differentiation, proliferation, and migration. It is also evident in association with the processes linked to embryogenesis during tissue development. In addition, tenascin is conserved as an important marker of tissue regeneration. It is possible that uterine fibroid may be associated with aberrantly regulated cell-ECM interactions. To assess this possibility, we determined the expression of tenascin by Western blot analysis in each human uterine fibroid and normal tissue. Using endometerial stromal cell cultured with and without tenascin, we investigated the expression patterns of collagen by immunocytochemistry, respectively. Mostly, the data showed that not only tenascin expression in uterine fibroids was higher than in normal tissues but also tenascin related to the production of collagen. These results suggest that tenascin contributes to uterine fibroid in endometrium. Therefore, we conclude that tenascin is one of the most important candidate markers in uterine fibroid. Program/Abstract # 81 Correlation of progressing human gastric intestinal metaplasia and fibrogenesis. Lee, Seulkina; Park, Younghun; Choi, Yunjeong; Park, Hyosang; Kim, Daeyoung; Hwang, Youjin (Incheon, Republic of Korea) Human gastric intestinal metaplasia (IM) is known for a disease progressed toward gastric cancer. IM is associated loss of E-cadherin and infection of H.pylori. Several types of IM is divided into complete IM (type 1 IM) and incomplete type II and III. But mechanism of IM is not well known. IM is presented by loss of activity in normal gastric epithelial cells caused by chronic gastritis that repeats damaging and recovering of cells. We studied correlation IM and fibrogenesis of human intestinal cells that similarly lose cells’ activities. We used several types of gastric IM patients’ stomach tissue samples and inflamed human intestinal cells. After that, using western blot analysis, we measured expression of cdx1, cdx2 gene that are realated IM regulation, TGF-β1 and IL-1β that are important factor of intestinal fibrogenesis in inflamed organs. And we calculated relevance of progress of IM to gastric cancer and fibrogenesis. Through this research, we confirmed correlation of change of morphology in intestinal metaplasia and fibrogenesis in intestine. It helps understanding embryologic development as well as in cancer and fibrosis. Program/Abstract # 82 Forward genetics reveals Xylt1 as a key, conserved regulator of bone development Mis, Emily K., Yale University Genetics, New HavenUnited States; Kong, Yong (Yale University, New Haven, United States); Liem, Karel (Yale University Pediatrics, New Haven, United States); Domowicz, Miriam; Schwartz, Nancy (Chicago, United States); Weatherbee, Scott (Yale University, New Haven, United States) Long bones form through the differentiation of mesenchymal cells into chondrocytes that form a cartilage template for the bone. Despite recent advances in understanding chondrocyte proliferation and maturation, many of the factors that regulate these steps are still unknown. Using massively parallel sequencing on a dwarf mouse mutant (pug), we identified Xylosyltransferase 1 (Xytl1) as a key regulator of chondrocyte maturation. Xylt1 is one of two xylosyl transferases found in vertebrates, which catalyzethe initial step in glycosylaminoglycan (GAG) synthesis. pug mutant limbs are shorter than normal limbs by birth, and those that survive display progressive shortening of their long bones throughout adulthood. Histological analyses revealed that pug mutants have reduced zones of differentiating chondrocytes, suggesting that proliferation or maturation could underlie the pug phenotype. We discovered that mutant skeletal elements displayed premature ossification, suggesting that early chondrocyte maturation contributes to the pug phenotype. The pug allele shows reduced xylosyl transferase activity, and consistent with the molecular function of Xylt1, we observed reduced GAG levels in pug mutants. Addition of GAG chains to proteoglycans is essential for normal signaling through multiple regulatory pathways. In pug mutants, reduced GAG levels result in increased short-range Ihh signaling, and expanded
27 Fgfr3 expression in the limb chondrocytes. Characterizing the pug mutant and defining the in vivo function of Xylt1 will greatly enhance our understanding of the signaling pathways and factors that coordinate skeletogenesis. Program/Abstract # 83 BMP heterodimer signaling in the developing vertebrate embryo Mullins, Mary; Dutko, James A. Perelman Sch of Med At Univ of Penn Cell & Developmental Biology, Philadelphia, United States The vertebrate embryonic dorsoventral (DV) axis is patterned by a bone morphogenetic protein (BMP) activity gradient. The BMP morphogen gradient is shaped primarily by the movement of BMP antagonists emanating from dorsal regions to ventral regions of the embryo. High BMP signaling levels arise ventrally whereas BMP antagonists attenuate signaling dorsally. In the zebrafish embryo, BMP signaling requires two ligands, Bmp2b and Bmp7a, functioning exclusively as a heterodimer, and their corresponding type I receptors, Alk3/6 and Alk8 (Alk2 paralog). Why BMP heterodimers function as the obligate ligand, while BMP homodimers, although present, fail to signal is an unanswered question and fundamental to the BMP signaling mechanism. Here we test one model for the obligatory function of BMP heterodimers in DV patterning: BMP antagonists preferentially block signaling by BMP homodimers. To test this model, we depleted Chordin, Noggin1, and Follistatin-like1b by injecting translation blocking morpholinos into bmp7a or bmp2b mutant embryos, i.e.,embryos devoid of BMP heterodimers. If BMP antagonists preferentially block signaling by BMP homodimers over heterodimers in vivo then we expect BMP homodimers to restore signaling when BMP antagonists are removed. Interestingly, no rescue was observed in embryos lacking BMP antagonists and BMP heterodimers. Thus, BMP heterodimers prevail during DV patterning by a mechanism other than a preferential block to BMP homodimers by BMP antagonists. We are currently investigating alternative hypotheses for the exclusive function of BMP heterodimers in DV patterning, including that BMP heterodimers bind to the receptor complex with a lower overall dissociation constant compared to BMP homodimers. Program/Abstract # 84 acal is a novel negative regulator of Drosophila JNK signaling during embryonic dorsal closure. Rios-Barrera, L. Daniel, Universidad Nacional Autonoma de Mexico (UNAM), Juriquilla, Mexico; Riesgo-Escovar, Juan R. (UNAM, Queretaro, Mexico) Dorsal closure is one of the last major morphogenetic rearrangements taking place during Drosophila embryogenesis. It consists of the stretching of the lateral epidermis towards the dorsal midline, and is controlled by the JNK signaling pathway. The only Drosophila JNK (encoded by basket) is activated at the most dorsal row of epidermal cells, from where it coordinates cell remodeling by inducing cytoskeleton modifications and signaling to adjacent cells. Mutants for JNK pathway genes die harboring a ‘dorsal open’ phenotype in cuticle preparations. In this work, we characterize a novel ‘dorsal open’ group gene, which we named acal. We generated an allelic series of acal mutants and mapped them to a nonannotated transcript with a low in silico protein coding capacity. We hypothesize that this transcript is a microRNA precursor. This contention is supported by high throughput RNA-sequencing by the modENCODE project. We also found that the transcript is enriched in nuclear preparations as expected for a nucleus-processed RNA. To get insight into the role of acal in JNK signaling, we analyzed genetic interactions of acal with basket mutants, and observed that basket mutations rescue acal defects. Similarly, JNK signaling target genes are ectopically expressed in acal mutants. These results show that Acal counteracts JNK signaling. acal is expressed in the epidermis, and its expression pattern is very similar to that of raw, another negative regulator of JNK signaling. Interestingly, acal expression is reduced in raw mutants, suggesting that Raw may act at least partially through Acal to downregulate JNK signaling during dorsal closure. Program/Abstract # 85 Notch controls daughter cell proliferation in Drosophila neural lineages Bivik, Caroline, Linkoping University, Linköping, Sweden While tremendous progress has been made with respect to the mechanisms controlling neural diversification, less is known regarding how the precise cell number of each neural sub-type is generated. The Drosophila embryonic CNS has been a valuable model for addressing these issues. The fly CNS is generated by a set of 1,000 progenitor cells, denoted neuroblasts, which form in the early embryo. Neuroblasts undergo repetitive rounds of asymmetric divisions, budding off daughter cells, before exiting the cell cycle after a distinct number of divisions. In most, if not all, early stages of lineage development, daughter cells divide once to generate two neurons/glia (Type I behavior). Recently, it has been demonstrated that some lineages display a proliferation switch, such that late-born daughters differentiate directly into neurons/glia (Type 0 behavior). As a consequence of these precise proliferation decisions each particular neuroblast generates a stereotyped lineage tree and lineage size. Thus, development of a lineage depends upon two fundamental
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
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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
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Page 23 and 24: 23 more likely than students who di
Page 25: 25 was a significant loss of cells
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Page 31 and 32: 31 and migration (ADAM13). They act
Page 33 and 34: 33 Program/Abstract # 101 The influ
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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
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Page 51 and 52: 51 malformations in murine limb bud
Page 53 and 54: 53 Yuqing (Mouse Imaging Centre, To
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Page 57 and 58: 57 Program/Abstract # 173 The role
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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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101 trafficking of cargo proteins a
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103 Sonic Hedgehog (Shh) is a secre
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105 tube was aberrant. Our data ind
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107 degradation of Smad proteins. W
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109 strong affects on organogenesis
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111 that maternally-supplied Lkb1 i
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113 Program/Abstract # 341 Coordina
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115 partners. Our transgenic gain o
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117 delayed and stunted as monitore
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119 Program/Abstract # 359 The meth
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121 Misregulation of molecular path
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123 back to the midbody in cbp-1 RN
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125 versus asymmetric cell division
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127 spinal cord. Iulianella, Angelo
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129 determine cell cycle activity i
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131 in expanded Lmx1a/b+ progenitor
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133 ROS levels. Collectively, our r
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135 limbs. Apoptosis was also pertu
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137 Henkels, Julia; Zamir, Evan, Ge
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139 however, and its role in CSF ma
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141 embryonic precursors to form an
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143 with fork retarding Replication
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145 homeodomain (HD) transcription
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147 fate, potentially acting downst
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149 involved in Drosophila ventral
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151 Program/Abstract # 456 Thoracic
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153 ureteric insertion into the bla
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155 of p16, a known cyclin kinase i
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157 rax mutant was recently found i
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Abstracts - Society for Developmental Biology

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