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Congress Abstracts - Society for Developmental Biology

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insights into the ancestral role of Nvlbx1 during endoderm differentiation in Nematostella. In Xenopus, our vertebrate model, we are<br />

using a combination of ChIP-Seq and RNA-Seq to determine potential Lbx1 binding sites and targets. The conserved gene regulatory<br />

network identified in our study should shed light on the evolution of myogenesis in metazoans.<br />

Program/Abstract # 301<br />

The TLR co-receptor TRIL is required <strong>for</strong> Spemann organizer function in Xenopus<br />

Xie, Yuanyuan (University of Utah, USA); Mimoto, Mizuho; Kwon, Sunjong (Oregon Health & Science University, USA); McKnite,<br />

Autumn; Christian, Jan (University of Utah, USA)<br />

Toll-like receptor (TLR) signaling plays an evolutionarily conserved role in innate immunity. The first identified TLR, Drosophila<br />

Toll, has an essential role in dorsal-ventral patterning, whereas a similar role <strong>for</strong> vertebrate TLRs has not been uncovered. I have<br />

shown that the novel transmembrane protein, TRIL, which was originally identified as a TLR co-receptor necessary to activate NF-kB<br />

in immune cells, is required <strong>for</strong> embryonic patterning in Xenopus. Xenopus TRIL is expressed in dorsal mesodermal cells that make up<br />

the Spemann organizer during gastrulation. Targeting TRIL antisense morpholinos to dorsal cells in Xenopus embryos causes<br />

gastrulation defects and spina bifida as well as loss of head and eyes at the tailbud stage. In situ hybridization and immunostaining<br />

analyses suggest that TRIL is required <strong>for</strong> <strong>for</strong>mation of the notochord and the central nervous system. Gene expression analyses show<br />

that TRIL regulates expression of a subset of organizer genes, including BMP antagonists, during gastrulation. We hypothesize that<br />

TRIL activates a TLR/NF-kB signaling pathway during gastrulation to regulate expression of BMP antagonists and other organizer<br />

genes required <strong>for</strong> neural induction and dorsal mesoderm <strong>for</strong>mation. These findings suggest that the role of Toll/NF-kB signaling in<br />

regulating expression of BMP antagonists required <strong>for</strong> dorsal-ventral axis <strong>for</strong>mation is conserved from flies to vertebrates.<br />

Program/Abstract # 302<br />

Fuz mutant mice reveal shared mechanisms between ciliopathies and FGF related syndromes<br />

Tabler, Jacqueline Marie (UT Austin, USA); Liu, Karen (King’s College London, UK); Walling<strong>for</strong>d, John (UT Austin, USA)<br />

Ciliopathies are a broad class of human disorders, with craniofacial dysmorphology as a common feature. Among the hallmarks of<br />

ciliopathies is high arched palate, a condition that impairs speech and reduces quality of life. We present here the ciliopathic Fuzzy<br />

mutant mouse as the first animal model of high arched palate. Using mouse and frog, we show that this defect arises not, as commonly<br />

suggested, from midface hypoplasia, but rather from increased neural crest expanding the first branchial arch, resulting in maxillary<br />

hyperplasia. High arched palate is also common in fibroblast growth factor (FGF) hyperactivation syndromes, and we find that<br />

craniofacial Fgf8 gene expression is significantly expanded in Fuz mutant mice. Moreover, genetic reduction of Fgf8 levels in Fuz<br />

mutant mice ameliorates the maxillary phenotypes. Finally, the mouse model of oral-facial-digital syndrome-1 (ofd1) also shows<br />

expanded domains of Fgf8 expression accompanied by an enlarged maxillary process, suggesting that aberrant FGF regulation is a<br />

common feature of ciliopathies. Thus, our findings reveal a cause <strong>for</strong> a common craniofacial anomaly and identify a novel etiological<br />

link between two classes of human disease: FGF-hyperactivation syndromes and ciliopathies.<br />

Program/Abstract # 303<br />

SUMOylated Sox3 is associated with chromatin and affects Sox3 function during zebrafish development<br />

Lam, Chi Man; Laghari, Zulfiqar Ali; Shih, Yu-Huan; Kuo, Cheng-Liang; Struebing, Silke; Scotting, Paul John (University of<br />

Nottingham, UK)<br />

Sox3 is a transcription factor participating in many developmental processes. However, it remains unclear how it is modified and<br />

regulated to function differently at certain times and locations in developing embryos. Our study investigates the role of Sox3<br />

SUMOylation. SUMOylation has been shown previously to have diverse effects on the activity of several transcription factors. Our<br />

previous results suggested that Sox3 directly represses organizer genes in zebrafish. Here we look at how the function of Sox3 on<br />

organizer <strong>for</strong>mation is regulated by SUMOylation. Our cell fractionation and western blot results demonstrated that SUMOylated<br />

Sox3 is associated with chromatin. Luciferase assays also demonstrated that SUMOylation of Sox3 alters its transcriptional activity<br />

and there<strong>for</strong>e enhances the repressing function of Sox3 on organizer <strong>for</strong>mation in zebrafish. Overall, these results suggest that<br />

SUMOylation of Sox3 is critical to control of its different activities during zebrafish development.<br />

Program/Abstract # 304<br />

Determining the role of an uncharacterized tubulin in the development of multiciliated epithelial cells in Xenopus laevis.<br />

Wills, Airon (University of Texas, Austin, USA), Turk, Erin (Stan<strong>for</strong>d, USA); Sedzinski, Jakub (University of Texas, Austin, USA);<br />

Howes, Stuart; Nogales, Eva (UC Berkeley, USA); Stearns, Tim (Stan<strong>for</strong>d, USA); Walling<strong>for</strong>d, John (University of Texas, Austin,<br />

USA)<br />

The tubulin superfamily is a well-conserved and ancient protein family. The most well-known members of this superfamily are alpha,<br />

beta, and gamma tubulin, which are found in all eukaryotes and <strong>for</strong>m the structure of the microtubule, and nucleate microtubules,<br />

respectively. However, a number of other tubulin family members have been variably inherited during evolution. Here, we present our<br />

study of a vertebrate tubulin that we have termed “eta-tubulin” due to its similarity with the eta-tubulin protein described in<br />

Paramecium. To our knowledge, eta-tubulin is the only member of the tubulin superfamily that remains completely uncharacterized in<br />

vertebrates. Here, we find that morpholino knockdown of eta-tubulin in Xenopus laevis embryos significantly shortens axoneme<br />

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