Abstracts - Society for Developmental Biology
Abstracts - Society for Developmental Biology
Abstracts - Society for Developmental Biology
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132<br />
Program/Abstract # 398<br />
From signals to shapes in tissue morphogenesis<br />
Shvartsman, Stas, Princeton University, United States<br />
The epithelial sheet that envelops the Drosophila oocyte gives rise to the eggshell, a complex structure that controls<br />
several critical aspects of embryonic development. Eggshell morphogenesis can be viewed as a two-step process, in which<br />
localized chemical cues induce highly robust tissue de<strong>for</strong>mations. In the first step, a small set of signals establish twodimensional<br />
expression domains of dozens of genes, which collectively control mechanical <strong>for</strong>ces and properties of cells<br />
across the epithelium. In the second step, these <strong>for</strong>ces act on the epithelium, trans<strong>for</strong>ming it into a three-dimensional<br />
structure. The anatomical simplicity of the developing egg makes it an ideal system <strong>for</strong> establishing multiscale models of<br />
epithelial morphogenesis. I will present the results of our ef<strong>for</strong>ts to develop and experimentally test quantitative<br />
descriptions of eggshell morphogenesis, starting from network biology of gene expression and then moving to<br />
biomechanical models of tissue de<strong>for</strong>mations.<br />
Program/Abstract # 399<br />
The enhancer disruption (ED) screen in zebrafish.<br />
Villar-Cerviño, Verona; Molano-Mazón, Manuel (U Miguel Hernandez, Spain); Catchpole, Timothy (UTSW Med Ctr);<br />
Valdeolmillos, Miguel (U Miguel Hernandez, Spain); Henkemeyer, Mark (UTSW Med Ctr); Martínez, Luis M.; Borrell,<br />
Víctor; Marín, Oscar (U Miguel Hernandez, Spain).<br />
Transposon-mediated enhancer trap screens in zebrafish have been reported as an effective way to screen <strong>for</strong> new genes<br />
involved in early developmental processes. Although this approach is well suited <strong>for</strong> the creation of gene reporter lines, it<br />
is relatively inefficient <strong>for</strong> the generation of mutations. Insulator sequences have been identified which can block<br />
transcription due to their interference with enhancer activity. We have exploited such insulating activity to build an<br />
innovative enhancer trap vector, based on the Tol2 transposon, whose mutagenic potential has been greatly enhanced by<br />
including an insulator sequence. As a classical enhancer trap, this tool is able to uncover genes with tissue-specific<br />
expression patterns and permit the isolation of their respective reporter lines. Moreover, due to its insulator activity, this<br />
transposon is also able to generate regulatory mutations through the disruption of tissue-specific enhancer activity.<br />
Additionally, we have incorporated the ability to discriminate between 5´and 3´enhancer activity relative to the<br />
transposon’s insertion point. Here we will present results of a genetic screen per<strong>for</strong>med with this tool which we refer to as<br />
an Enhancer Disruption (ED) vector and will discuss its efficient mutagenic activity and its impact in genomic regulatory<br />
landscapes.<br />
Program/Abstract # 400<br />
Cellular tiling in the cerebral cortex through contact repulsion<br />
Bessa, José; Luengo, Mario; Rivero-Gil, Solangel; Ariza-Cosano, Ana; Naranjo, Silvia; Campaña, Francisco;<br />
Caballero, Pablo; Gómez-Skarmeta, José Luis, Centro Andaluz de Biología del Desarrollo, Spain<br />
Cajal-Retzius (CR) cells play a fundamental role in the development of the mammalian cerebral cortex. They control the<br />
<strong>for</strong>mation of cortical layers by regulating the migration of pyramidal cells through the release of Reelin. The function of<br />
CR cells critically depends on their disposition throughout the surface of the cortex, but little is known about the events<br />
controlling this phenomenon. We found that migrating CR cells repel each other upon contact, which leads to their random<br />
dispersion throughout the cortical surface and to the <strong>for</strong>mation of a dynamically stable pattern of distribution that optimizes<br />
surface coverage. This process of cellular tiling is mediated by bi-directional Eph/ephrin interactions. Our observations<br />
reveal a novel mechanism that controls the even distribution of neurons in the developing brain.<br />
Program/Abstract # 401<br />
Capicua regulates proliferation and survival of RB-deficient cells in Drosophila.<br />
Krivy, Kate; Bradley-Gill, Mary-Rose; Moon, Nam, McGill University, Montreal, Canada<br />
Mutations of rbf1, the Drosophila homolog of the RB tumour suppressor gene, generate defects in cell cycle control,<br />
differentiation and cell death during development. Previous studies have established that EGFR/Ras activity is an<br />
important determinant of proliferation and survival of rbf1 deficient cells. Here, we report that Capicua (Cic), an HMG<br />
box transcription factor whose activity is regulated by the EGFR/Ras pathway, regulates both survival and proliferation of<br />
rbf1 mutant cells. We demonstrate that cic mutations allow rbf1 mutant cells to bypass developmentally controlled cell<br />
cycle arrest and apoptotic pressure. The cooperative effect between Cic and RBF1 in promoting G1 arrest is mediated, at<br />
least in part, by limiting Cyclin E expression. Surprisingly, we also found evidence to suggest that cic mutant cells have<br />
decreased levels of Reactive Oxygen Species (ROS), and that the survival of rbf1 mutant cells are affected by changes in