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Congress Abstracts - Society for Developmental Biology

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conserved in amniotes other than chick? We are currently exploring axis <strong>for</strong>mation in reptiles, focusing on chameleon (Squamata) and<br />

turtles (Testudines).<br />

Program/Abstract # 350<br />

Building a Vertebrate Embryo Using a Combination of Morphogenetic Gradients<br />

Xu, Peng-Fei; Ferri, Karine; Thisse, Christine; Thisse, Bernard (University of Virginia, USA)<br />

We have previously shown that in zebrafish, the entire embryonic margin acts as a global and continuous organizer. The organizing<br />

properties result from the combined activity of BMP and Nodal morphogenetic gradients and the gradual variation of their ratio of<br />

activity observed from the ventral to the dorsal domains of the margin is the crucial parameter that controls the identity of the<br />

embryonic structures <strong>for</strong>med. By recapitulating, within the field of uncommitted blastomeres of the animal pole, the continuous<br />

variation of BMP/Nodal ratio of activities observed at the embryonic margin, we are able to induce the <strong>for</strong>mation of a complete<br />

secondary embryo that contains all tissues and organs of a wild-type embryo and that develops at the animal pole from animal pole<br />

cells. Analysis of the respective contribution of the BMP and Nodal pathways to the <strong>for</strong>mation of the secondary embryo reveals that<br />

Nodal signalling results in the <strong>for</strong>mation of a blastopore where an ectopic gastrulation occurs leading to the <strong>for</strong>mation of radially<br />

symmetrical structures of dorsal identity. Adding a BMP secreting centre adjacent to the domain stimulated by Nodal breaks the<br />

symmetry of the blastopore lip, inducing ventral and lateral tissues to <strong>for</strong>m and in addition that polarizes gastrula cell movements. Our<br />

analysis reveals that the antero-posterior orientation of the ectopic embryonic axis depends only on the position of the BMP secreting<br />

cells relative to the blastopore induced by Nodal and is completely independent of the primary embryo. Altogether, our study<br />

establishes that, artificially imposing these morphogenetic gradients to receptive, yet uncommitted cells, is sufficient to turn on and<br />

control the zygotic developmental pathways responsible <strong>for</strong> the <strong>for</strong>mation of a whole embryo and supports that the main function of<br />

the maternally provided spatial determinants is to induce and/or stabilize the morphogenetic gradients of BMP and Nodal.<br />

Program/Abstract # 351<br />

Role of FGF signaling in maintenance of cardiac chamber identity in zebrafish<br />

Pradhan, Arjana; Zeng, Xin-Xin (Univ of Cali<strong>for</strong>nia, San Diego, USA); Marques, Sara (Skirball Institute of Biomolecular Med, NYU<br />

School of Med, USA); Chi, Neil; Yelon, Deborah (Univ of Cali<strong>for</strong>nia, San Diego, USA)<br />

The heart is composed of two types of cardiac chambers, atria and ventricles, each of which behaves as a distinct functional subunit<br />

with unique morphological, electrophysiological, and contractile properties. Hence, the proper chamber-specific differentiation of<br />

atrial and ventricular cardiomyocytes is crucial <strong>for</strong> the <strong>for</strong>mation of a functional heart. Although there is some understanding of the<br />

pathways important <strong>for</strong> initiating chamber-specific differentiation, little is known about the pathways required to maintain identities of<br />

differentiated cardiomyocytes. In previous studies, we have demonstrated that fibroblast growth factor (FGF) signaling facilitates the<br />

initial <strong>for</strong>mation of ventricular cardiomyocytes. Here we show that FGF signaling is also required after the initial differentiation of<br />

ventricular cells in order to preserve ventricular identity. We find that both pharmacological and genetic inhibition of FGF signaling<br />

can generate ectopic atrial cardiomyocytes within the already differentiated ventricle. Analysis using chamber-specific reporter<br />

transgenes suggests that these ectopic cells are produced through transdifferentiation of ventricular cardiomyocytes. In addition, we<br />

find that administration of retinoic acid (RA) can disrupt ventricular chamber identity, suggesting the possibility of a genetic<br />

interaction between the FGF and RA pathways. Together, our data suggest a model in which differentiated ventricular<br />

cardiomyocytes retain some plasticity and require continuous FGF signaling to preserve their chamber-specific identity. Ongoing<br />

work will identify the molecular pathway through which FGF signaling acts in this context.<br />

Program/Abstract # 352<br />

Modulation of fungi<strong>for</strong>m papillae patterning by Fgf signaling<br />

Prochazkova, Michaela (UCSF, USA), Häkkinen, Teemu (University of Helsinky, Finland); Prochazka, Jan; Jheon, Andrew (UCSF,<br />

USA); Jervall, Jukka (University of Helsinky, Finland); Klein, Ophir (UCSF, USA)<br />

Introduction: Fungi<strong>for</strong>m papillae are epithelial structures that house taste buds on the anterior tongue. Many molecular pathways are<br />

known to influence the patterning of the fungi<strong>for</strong>m papillae. Canonical Wnt signaling was shown to initiate fungi<strong>for</strong>m papillae<br />

<strong>for</strong>mation, whereas other pathways triggered by Shh, Egf or Bmp have inhibitory effects on papilla size and number. However,<br />

mesenchyme-derived signaling factors have not yet been identified, hampering the development of a comprehensive model of papilla<br />

patterning. Results: We have examined the role of Fgf10 in fungi<strong>for</strong>m papilla development. Evaluation of Fgf10 and Spry2 knockout<br />

phenotypes showed that Fgf10, which is expressed in the tongue mesenchyme underlying the papillary field, functions as a negative<br />

regulator of fungi<strong>for</strong>m papilla size. Using BATGAL mice, we demonstrated that this role is mediated by inhibition of canonical Wnt<br />

signaling, which is the main activator of papilla development. A gene expression analysis using qRT-PCR revealed interactions<br />

between Fgf10 and the Wnt and Shh pathways. We then represented these results mathematically using a reaction-diffusion model to<br />

simulate activator-inhibitor dynamics in the system. Summary: Fgf10 functions as a negative regulator of fungi<strong>for</strong>m papilla size<br />

during embryonic development, suggesting a role in fine-tuning taste sensitivity. The proposed mechanism of Fgf10 action is via<br />

inhibition of canonical Wnt activity. FGF10 is the first mesenchyme-derived factor to date involved in fungi<strong>for</strong>m papillae patterning.<br />

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