Congress Abstracts - Society for Developmental Biology

owser. The genomic differences observed were the following: 2/10 healthy individuals showed copy number variants (CNV)
consisted of gains in 3p12.3, 9q21.11 and 17q21.31, and loss in 4q13.2. In T21 patients with CHD we observed a gain in 9q21.11, loss
of heterozygocity (LOH) in 10p12.31 and 19q13.2. In T21 patients without CHD we observed LOH in 4q13.3, 6p22.1, 8q22.22, 15
q13.3, 16q22.1 and loss in 4q13.3 and 14q11.2. In T21 abortions we detected LOH in the regions 4p15.1, 10p12.31 and 20q11.21. The
most evident difference among the groups is that live births either T21 or controls, had some regions with CNV that are absent in T21
abortions, this CNV could balance the extra chromosome 21 in live births, while in abortions its absence could compromise the
normal development. Our study contributes to find possible reasons for trisomy 21 embryo survival.
Program/Abstract # 267
Microarray analysis of the embryonic skull vault.
Barrell, William; Healy, Christopher (Craniofacial Development and Stem Cell Biology, UK); Ota, Masato (Section of Molecular
Craniofacial Embryology, Japan); Ohazama, Atsushi (Craniofacial Development and Stem Cell Biology, UK); Dionne, Marc (Centre
for the Cellular and Molecular Biology of Inflammation, UK); Liu, Karen (Craniofacial Development and Stem Cell Biology, UK)
The mammalian skull vault is formed from two distinct embryonic cell populations, with the frontal bones and intervening suture
arising from neural crest cells whereas the parietal bones are mesodermally derived. The coronal suture, which separates the frontal
and parietal bones, is of mixed origins. As the brain grows the skull must be able to accommodate the increasing size, therefore it is
crucial for the timing of ossification and suture fusion to be tightly regulated. Previous reports on postnatal bones suggest that
differential gene expression is correlated with the different embryonic origins. However, there have been few unbiased analyses
focusing on embryonic expression patterns. In this study, we have performed microarray analyses on dissected frontal and parietal
bones, interfrontal and coronal sutures at 15.5 and 18.5 days post coitum (DPC). We then performed pairwise analyses between tissues
and time points, as well as hierarchical clustering of the differentially expressed genes. In addition, gene ontology (GO) process
analysis is presented, revealing dynamic changes during skull vault formation. Finally, by comparing expression in frontal and parietal
bones, we identified high levels of sclerostin domain-containing protein 1 (Sostdc1) in the frontal bone at 15.5DPC. Sostdc1 is a
secreted protein reported to inhibit both the BMP and Wnt signaling pathways. Microcomputed tomography (mCT) and cephalometric
measurements revealed that Sostdc1 knockout mice have altered skull shapes compared to wildtype controls. All together, our data
provide a springboard for further analyses of the dynamic changes necessary for proper development of the embryonic skull vault.
Program/Abstract # 268
Interactions Between Organizer Genes and Early Neural Ectodermal
Klein, Steven L. (National Science Foundation, USA); Moody, Sally; Neilson, Karen (George Washington University, USA)
Neural induction involves Organizer inhibition of factors that repress neural genes: BMP, Wnt & Nodal. However, Organizer genes
probably activate early neural ectodermal genes as well. We previously determined the transcriptional relationship between 4 early
neural ectodermal genes that form a gene regulatory network controlling the progression of neural ectodermal precursors to neural
stem/progenitor cells. We next studied the interactions between these neural genes, and the Organizer genes to provide a morecomplete
view of neural induction. We used an ectopic induction assay by expressing Organizer genes in Xenopus blastomere
precursors of epidermis and assaying the expression of FoxD4L1, Sox11, Gmnn, & Zic2 by ISH at neural plate stages. We found that
the factors that induced FoxD4L1/Sox11 & Gmnn/Zic2 were not identical. Induction of FoxD4L1 & Sox11 required blocking BMP &
Wnt signaling, whereas Gmnn & Zic2 were induced by blocking only Nodal or BMP. FoxD4L1 & Sox11 were only induced by Siam
& Twn, whereas Gmnn & Zic2 were induced by Siam & Twn, which partially required FoxD4L1 activity, as well as by Lim1, FoxA4,
Otx2 & Pou2. FGF but not Nodal was required for the Siam-mediated induction of all 4 genes. These findings show that two
independent pathways lead to neural gene expression. In one, Siam/Twn activate FoxD4L1 transcription, directly and indirectly via
FGF signaling and in the absence of both BMP & Wnt signaling, and FoxD4L1 in turn activates Sox11, Gmnn & Zic2. In the second,
Gmnn & Zic2 are activated by other Organizer factors, both directly and indirectly in the absence of BMP and/or Nodal. These studies
provide greater detail of the molecular interactions that regulate the induction of neural ectoderm.
Program/Abstract # 269
To be or not to be - mutually exclusive neural and non-neural ectodermal competence territories are established at the neural
plate border
Schlosser, Gerhard (National University of Ireland), Pieper, Mareike; Ahrens, Katja (Brain Research Institute, University of Bremen,
Germany)
Cranial placodes give rise to many sensory organs and ganglia of the vertebrate head. All placodes are now known to arise from a
common panplacodal primordium located around the anterior neural plate. It has been proposed that this primordium and the neural
crest arise from a common precursor, the neural plate border region. However, using tissue grafting in Xenopus embryos we show that
during gastrulation two mutually exclusive competence territories are established at the neural plate border. Whereas competence for
induction of neural plate, neural plate border and neural crest markers is confined to neural ectoderm, competence for induction of
panplacodal markers is confined to non-neural ectoderm. We also show that Dlx3 and GATA2 are required cell-autonomously for
panplacodal and epidermal marker expression in the non-neural ectoderm, while ectopic expression of Dlx3 or GATA2 in the neural
plate suppresses neural plate, border and crest markers. Overexpression of Dlx3 (but not GATA2) in the neural plate is sufficient to
induce different non-neural markers in a signaling dependent manner, with epidermal markers being induced in the presence, and
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