s / Developmental Biology 331 (2009) 517–529 occurred. Overexpression of TBX22 caused a striking decrease in proliferation but did not change the level of apoptosis. Furthermore we identified two targets of TBX22 that could be mediating the phenotype, DLX5 and MSX2. We have therefore demonstrated novel functions for TBX22, a gene that causes some forms of human orofacial clefting. This work was funded by CIHR grants to JMR. doi:10.1016/j.ydbio.2009.05.521 Program/Abstract # 494 A point mutation in Arid1a reveals an essential role for this SWI/SNF subunit in extraembryonic blood vessel and trophoblast development Ronald L. Chandler, Jennifer Brennen, Terry Magnuson Department of Genetics, University of North Carolina, Chapel Hill, NC, USA Arid1a is a signature subunit of the mammalian SWI/SNF ATP- dependent chromatin remodeling complex. We performed an ENU mutagenesis screen for Arid1a coding mutations and generated mice carrying a valine-to-glycine point mutation in the ARID DNA binding domain of Arid1a. Although mutant protein is expressed near wild- type levels and capable of interacting with its catalytic subunit, Brg1, it appears to display reduced DNA binding capacities in vitro. Homozygous mutant embryos undergo development arrest by E10.5 and exhibit defects in the trophoblast placenta and extraembryonic vasculature, including a compacted labyrinth layer and reduced vascular branching. These data suggest the ARID domain of Arid1a is essential for development. doi:10.1016/j.ydbio.2009.05.522 Program/Abstract # 495 The role of Friend of GATA in primitive red blood cell development Mizuho S. Mimoto, Jan L. Christian Department of Cell and Developmental Biology, Oregon Health and Science University, Portland, OR, USA The transcription factor GATA-1 and its cofactor Friend of GATA (FOG) are required to promote embryonic red blood cell (RBC) development in mice. In contrast, the current model in Xenopus, based on overexpression studies, predicts that FOG inhibits RBC development by recruiting the transcriptional co-repressor C- terminal Binding Protein (CtBP). To resolve these seemingly contra- dictory findings, we have used morpholinos to perform a loss-of- function study in frogs. We find that in Xenopus, as in mice, FOG is in fact required for RBC development. Specifically, targeted injection of FOG morpholinos into the ventral blood-forming mesoderm of 8-cell Xenopus embryos results in a dose-dependent loss of globin expression at the tailbud stage. In addition, we find that over- expression of both wildtype FOG and mutant FOG isoforms that either lack known repressor binding domains, or harbor mutations at key GATA-interaction residues, also result in loss of blood. Together, these studies suggest that FOG is required for RBC development and that loss of blood seen with FOG overexpression is likely due to a dominant-interfering effect by which excess FOG sequesters other co-factors required for RBC development away from endogenous target promoters. Specific domains of FOG required for RBC development in vivo have not yet been elucidated. We are currently asking whether various FOG mutant constructs can rescue RBC formation in FOG morphants. This will allow us to determine which functional domains of FOG are required for normal erythropoiesis, and may suggest novel binding partners that are important for FOG's role during RBC development. doi:10.1016/j.ydbio.2009.05.523 Program/Abstract # 496 Stacked expression of Hand2 and Dlx mediates signaling from Edn1 to produce discrete pharyngeal arch patterning domains Jared Coffin Talbot, Charles B. Kimmel Institute of Neuroscience, University of Oregon, Eugene, OR, USA Recent studies have suggested that Endothelin1 (Edn1) acts in a dose dependent fashion to pattern skeleton from the first two pharyngeal arches into dorsal, intermediate, and ventral domains via its targets hand2 and Dlx. We hypothesized that hand2 expression defines the ventral domain, in part by repressing intermediate domain genes. We further hypothesized that Dlx genes pattern the intermediate domain. Third, we propose that the combined patter- ning from hand2 and Dlx delineates ventral/intermediate domains from dorsal. Here we demonstrate that hand2 is expressed next to edn1, and the expression of all Dlx genes extends dorsal to hand2. We provide evidence that dlx3b, dlx4b, and dlx5a are redundantly required for intermediate domain patterning. Furthermore we show that by 36 hpf, dlx3b, dlx4a, and dlx4b are specifically expressed in intermediate arch mesenchyme. Previous work demonstrated that hand2 is required for ventral cartilage formation. We confirmed this with two alleles of hand2. We further show that in hand2 mutants, dlx3b, dlx4a, and dlx4b expression expands into the ventral domain at 36hpf. Finally, when Dlx-MO is injected into hand2 mutants, both ventral and intermediate defects are seen, and the ventral-most structures may acquire dorsal shape. Collectively our work suggests that the stacked expression of hand2 and Dlx mediates signaling from Edn1 to generate ventral and intermediate domains with distinct identities separate from dorsal. (Supported by NIH grants DE13834 and DTG GM007257). doi:10.1016/j.ydbio.2009.05.524 Program/Abstract # 497 A follistatin-BMP7 feedback circuit controls taste papillae development and patterning in mouse tongue Piper L. Hollenbeck a,d , Crestina Beites a , Joon Kim a , Robin Lovell-Badge e , Scott Christley c,d , Qing Nie c,d , Arthur Lander b,d , Anne Calof a,b,d a Department of Anat. and Neuro., UC Irvine, Irvine, CA, USA b Department of Dev. and Cell Bio., UC Irvine, Irvine, CA, USA c Department of Math., UC Irvine, Irvine, CA, USA d Center for Complex Biological Systems, UC Irvine, Irvine, CA, USA e Department of Dev. Genetics, NIMR-MRC, London, UK Interactions between epithelium and mesenchyme are thought to drive development and patterning of taste papillae, but the identities of the mesenchymal signals are unknown. Using mouse genetics, we show that Fst, which is expressed in tongue mesenchyme during development, controls these processes in both anterior (normally gustatory) and posterior (normally non-gustatory) lingual epithelium. In anterior Fst −/− tongue there are increased numbers of Sox2+ taste progenitors, with fungiform papillae of abnormal size and spacing. In posterior Fst −/− tongue, ectopic Sox2+ epithelial domains develop and non-gustatory filiform papillae are absent. Increased Bmp7 expression is evident in regions of ectopic Sox2+ progenitors, and