| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Research Abstract |
Although steroid hormone regulates many important biological phenomenon, such as development and home, pstasis, it is not well understood how apoptosis is regulated by steroid hormone. In Drosophila, it is known that apopkosis is regulated in development by an insect steroid hormone, 20-hydroxyecdysone. We established cell lines derive from the cells of Drosophila larval central nervous system. Among these cell lines, some cell lines show the char, cteristics of larval types of central nervous system and some other cell lines show those of adult types of central nervous system. Therefore, the cell lines are used for various studies related with development and cell biology. Using these cell lines and other Drsophila embryonic cell lines as a model system, we investigated the mechanism of apoptosis induced by addition or deprivation of 20-hydroxyecdysone. Steroid hormone has been shown to act as a transcription factor. It was revealed that 20-hydroxyecdysone also regulates the expression of Drosophila cell death genes, reaper and hid. Although the changes of expression levels were differently regulated among the cell lines, the levels of both genes were consistently increased when apoptosis was occurred. The expression patterns of the subtypes of receptors for 20-hydroxyecdysone, EcR-A and EcR-B, were also different among the cell lines. The RNA interference experiments for EcR-A or EcR-B showed that apoptosis was inhibited by 20-hydroxyecdysone through EcR-A, whereas apoptosiswas induced through EcR-B.Theseresults indicatedthatapoptosisisregulated by 20-hydroxyecdysone, and the subtype of 20-hydroxyecdysone receptors expressed in a cell control the expression of cell death genes. In addition, we also investigated the mechanism of apoptosis by the over-expression experiments of cell death genes.
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