Abstracts Stem cells and tissue regeneration Program/Abstract # 270 The zebrafish laf/alk8 mutant as an in vivo model for molecular dissection of replacement tooth formation Pamela C. Yelick 3 , Ann Huysseune 1 , R. Craig Albertson 1 Department of Biology, Ghent University, Ghent, Belgium 2 Department of Biology, Syracuse University, Syracuse, NY 13244, USA 3 Division of Craniofacial and Molecular Genetics, Department of Oral and Maxillofacial Pathology, Tufts University, Boston, MA 02111, USA Zebrafish exhibit continuous replacement tooth formation in a manner very similar to adult tooth formation, providing the means to elucidate molecular signaling cascades regulating this process. The zebrafish alk8 mutant lost-a-fin (laf/alk8) is a valuable model for replacement tooth formation. Although homozygous recessive laf/alk8 mutants exhibit an early lethal phenotype, heterozygous laf/alk8 mutants are viable and fertile, but do not form replacement teeth. We are currently elucidating alk8 downstream signaling partners participating in primary and replacement tooth formation. Our studies in zebrafish comple- ment mammalian tooth tissue engineering studies currently being performed in this laboratory. We anticipate that the proposed studies in zebrafish will likely result in the identifica- tion of molecular signaling networks mediating replacement tooth formation in the zebrafish, which may facilitate the crea- tion of clinically relevant, molecular based replacement tooth therapies in humans. Supported by NIH/NIDCR grants DE1 2076, DE12024, and RO1 DE018043. doi:10.1016/j.ydbio.2007.03.570 Program/Abstract # 271 The role of IP 3 signalling during embryonic wound healing in Xenopus Ximena Soto 1 , J. Sivak 2 , L. Petersen 2 , E. Amaya 1 1 The Healing Foundation Centre, University of Manchester, Manchester M13 9PT, UK 2 The Gurdon Institute, University of Cambridge, Cambridge CB2 1QN, UK A major goal in regenerative medicine is to understand and ultimately facilitate our body's ability to repair itself following injury. We have begun to investigate the molecular and cellular basis of embryonic wound healing, given that embryos have the capacity to heal wounds quickly and completely. Tissue repair resembles embryo morphogenesis in several ways, including cell migration, proliferation and differentiation. In a screen for genes involved in morphogenesis in Xenopus, we identified an Ins(1,4,5)P 3 phosphatase (IP 3 P), which impairs embryonic wound healing, suggesting that Ins(1,4,5)P 3 (IP 3 ) signalling plays a role in this process. This finding has motivated us to investigate the role of IP 3 signalling during embryonic wound healing, using Xenopus as a model system. Two sets of enzymes regulate this pathway, the Ins(1,4,5)P 3 3-kinases (IP 3 K) and IP 3 P. IP 3 P, such as IP 3 P-5, promote Ins(1,4)P 2 (IP 2 ) generation, which is an inactive product, while IP 3 K generate Ins(1,3,4,5)P 4 (IP 4 ), which is involved in calcium release modulation. We have cloned IP 3 K B and IP 3 P-5 A from X. tropicalis and have begun to investigate their temporal and spatial patterns of expression. In addition, we are misexpressing these genes and modulating the activity of IP 3 K during early development in order deter- mine the effect of modulating IP 3 levels in embryonic wound healing assays. Finally we are investigating the consequence of these manipulations on the organization of the cytoskeleton. The aim of these studies will be to understand the role of IP 3 signalling in embryonic wound healing. doi:10.1016/j.ydbio.2007.03.571 Program/Abstract # 272 Strain and age differences in ear wound healing in mice Cláudia R. Carvalho 1 , Raquel A. Costa 1 , Geraldo M. Azevedo-Junior 3 , Valéria Ruiz-de-Souza 1 , Nelson M. Vaz 2 1 Dept of Morphol, ICB-UFMG, MG, Brazil 2 Dept of Immunol, ICB-UFMG, MG, Brazil 3 Public Hospital, Betim, MG, Brazil Small (2 mm) round holes in the ears of MRL and nude mice tend to close with characteristics of regeneration believed not to Developmental Biology 306 (2007) 390 – 395 www.elsevier.com/locate/ydbio doi:10.1016/j.ydbio.2007.03.302