| Summary: | 碩士 === 國立臺灣師範大學 === 生命科學系 === 97 === Raw, a component of djnk signaling pathway, plays a role in dorsal closure by modulating expression of Dpp in epidermal cells at the leading edge. The expression domain of Dpp was found to be markedly expanded in raw mutant embryos at stages 12-14. Similar to a previous study, we found that deficit in raw causes overproduction of cardial precursor cells in Drosophila at stages 13-14 which is concurrent with the ectopic Dpp activity. This result can be explained because mesodermal overexpression of dpp has shown to promote formation of cardial precursors. Nevertheless, various cardial cells are disappeared in raw mutant embryos at stages 15-16. We hypothesized that loss of cardial cell is resulted from apoptosis in late raw mutants. Indeed, excessive cell death, particularly in dorsal ectoderm and dorsal mesoderm, were observed in raw mutant embryos. Since the distribution of apoptotic cell coincides well with both the spatial and temporal expression domain of ectopic dpp, suggesting that ectopic dpp may induce cardial cell apoptosis in Drosophila. We show that increasing in Dpp activity alone promotes apoptosis in dose-dependent manner. In addition, we show that Dpp induced apoptosis is mediated through dTAK1, as mesodermally expression of a dominant negative dTAK1 suppresses apoptosis of cardial cell in raw mutation embryos. Interestingly, dTAK has shown to activate expression of djnk and dpp. This means that djnk signaling is constitutively activated in mesoderm by ectopic dpp from dorsal ectoderm. We have further demonstrated mesodermal dTAK1 induced apoptosis can be suppressed by expression of dominant negative p53. Since BMP signaling pathway induces apoptosis has also been shown to be mediated through TAK1 in mammals. Thus, the BMP induced apoptosis pathway may be evolutionarily conserved.
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