| Project/Area Number |
12480223
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Developmental biology
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
AGATA Kiyokazu Faculty of Science, Okayama University, Professor, 理学部, 教授 (70167831)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,500,000 (Direct Cost: ¥14,500,000)
Fiscal Year 2001: ¥4,800,000 (Direct Cost: ¥4,800,000)
Fiscal Year 2000: ¥9,700,000 (Direct Cost: ¥9,700,000)
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| Keywords | planarian / RNAi / Morphogenesis / regeneration / receptor / gene knockout / 転写因子 / シグナル分子 / ホメオポックス |
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| Research Abstract |
The planarian regeneration system offers the potential to allow us to understand how we can rebuild organs and tissues after any injuries, diseases or ageing. These high regenerative abilities are based upon the proliferation and differentiation of a population of totipotent stem cells called neoblasts. Here we show the role of a novel gene, Djndk, in anteroposterior patterning of the CNS. Djndk encodes a FGF receptor-like protein, and is expressed in the head region. Surprisingly, loss-of-function of Djndk by RNAi initiates ectopic formation of brain tissues with eyes in the posterior region of regenerating fragments as well as an intact body of planaria. Furthermore, this ectopic brain formation is suppressed by inhibition of both FGF receptor genes 1 and 2, and also by X-ray irradiation that causes disruption of totipotent stem cells. Djndk was also found to inhibit FGF signalling as assayed by mRNA injection experiments with Xenopus embryos and animal ectoderm treated with FGF. These data suggest the possibility that Djndk directly or indirectly interacts with FGF signalling to prevent the totipotent stem cells from developing into brain tissue in the trunk and tail region.
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