Abstracts - Society for Developmental Biology

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studied processes, open new fields of insect research to functional analysis and finally are developing Tribolium into a
complementary screening platform. We established a screening procedure for two parallel screens, which allows the rapid,
efficient identification of genes involved in embryonic or postembryonic development. After having screened about half of
the Tribolium genome, we can conclude that more than half of the genes show an effect in our assays. We identified novel
genes required for segmentation, axis formation, head development and oogenesis. New factors involved in muscle
development are being further analyzed in Drosophila and newly identified genes essential for survival, metamorphosis
and odoriferous gland biology will be of great interest for many scientists beyond the Tribolium community. Thus we show
that Tribolium truly developed into a powerful model for unbiased screening approaches.
Program/Abstract # 54
A blueprint for heart regeneration
Poss, Ken, Duke University,Durham, United States
By contrast with adult mammals, zebrafish regenerate cardiac muscle after major injury. In recent studies, we used genetic
fate-mapping to reveal that this regeneration occurs through activating proliferation of pre-existing cardiomyocytes at sites
of injury. Yet, the molecular mechanisms by which injury activates cardiomyocyte proliferation remain elusive. Here, we
have used new technologies to identify cardiac cell type-specific gene expression profiles during heart regeneration. Our
findings indicate key injury responses that enable cardiomyocyte proliferation and new muscle regeneration.
Program/Abstract # 55
Imparting regenerative capacity to limbs by progenitor cell transplantation
Lin, Gufa; Chen, Ying; Slack, Jonathan (U Minnesota, Minneapolis, United States
Some vertebrate animals, mostly urodele amphibians, can regenerate limbs after amputation while others cannot. Until now
it has not been possible to impart regenerative capacity to animals that cannot do it. The frog Xenopus can normally
regenerate its limbs at early developmental stages but loses the ability in the late tadpole such that postmetamorphic frogs
can only produce an unsegmented cartilaginous spike after amputation. This behavior provides a potential gain-of-function
model for measures that can enhance limb regeneration. However, all previous attempts to stimulate frog limb regeneration
have been unsuccessful or proved irreproducible. Here we show that frog limbs can be caused to form multi-digit
regenerates after receiving transplants of larval limb bud cells supplemented with suitable factors. We show that limb bud
cells can promote frog limb regeneration, but that success requires the activation of Wnt/beta-catenin signaling in the cells,
plus the provision of the exogenous factors Shh, FGF10 and thymosin beta 4. These factors promote survival and growth
of the grafted cells and also provide pattern information for the forming limb structures. The eventual regenerates are not
composed solely of donor tissue; the host cells also make a substantial contribution despite their lack of regenerationcompetence.
Cells from adult frog legs or from regenerating tadpole tails do not promote limb regeneration, demonstrating
the necessity for limb bud cells. These findings have obvious implications for the development of a technology to promote
limb regeneration in mammals. (G. L. and Y. C. contribute equally to this work)
Program/Abstract # 56
Mitotic neurons: failure to withdraw from the cell cycle produces anterograde transport of nuclei and
nonautonomous neuronal toxicity
Baker, Nicholas E., Albert Einstein College of Medicine, Bronx, United States
Neurons are such a firmly postmitotic cell type, so rarely forced back into the cell cycle even experimentally that little is
known about the mechanisms of their cell cycle withdrawal. We have discovered mutations in three Drosophila genes of
related function that cause a class of retinal photoreceptor neurons to continue dividing even after their specification and
differentiation has begun. These cells execute a remarkable cell cycle in which they lack well-formed cleavage furrows and
cytokinesis is replaced by transport of one daughter nucleus into the axons and towards the central brain. The transport
depends on kinesin, resembling the anterograde axonal transport of vesicles. Many of these abnormal neurons degenerate
before the adult fly emerges. Unexpectedly, genetic mosaic analysis shows that they also cause the loss of many of the
neighboring neurons whose cell cycle has usually been normal. This novel syndrome of mitotic neurons suggests
connections between cell cycle defects, axonal trafficking, and syndromes of progressive neuronal loss. It will be
interesting to discover whether it is the development of an axon that is incompatible with cytokinesis in neurons, and
whether such cell cycle defects cause neuronal cell loss in any neurodegenerative diseases.
Program/Abstract # 57
Growing organs communicate and adapt their growth programs and maturation to ensure final correct size via a
novel Drosophila Insulin-like peptide