2001 Fiscal Year Final Research Report Summary
A study of mechanisms involved in JNK pathway activation during Drosophila development.
| Project/Area Number |
12680707
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | OSAKA BIOSCIENCE INSTITUTE |
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Principal Investigator |
ISHIMARU Satoshi Osaka Bioscience Institute, Director's Lab, Research Associate, 所長研究部, 研究員 (00203026)
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| Project Period (FY) |
2000 – 2001
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| Keywords | Crk / C3G / CAS / Dock180 / Myoblascity / RNA interference / thorax closure / Drosophila / reverse genetics |
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| Research Abstract |
We analysed the loss-of-function-function phenotypes of Crk and its SH3 binding molecules, C3G and Docki 80 during Drosophila development. Especially, we wanted to know whether they were involved in the activation of JNK pathway, because ectopic expression of Drosophila C3G (DC3G) during Drosophila embryogenesis caused the over-activation of JNK. In this project, we decided to see the loss-of-function phenotypes of Drosophila Crk (DCrk), DC3G and Myoblast city (A Drosophila Dock180 homolog) by using inducible and heritable RNA interference (RNAi) method. We found that all of them are involved in thorax closure for which JNK pathway is also required. We identified a very promising candidate for an upstream receptor of Crk signaling pathway during thorax closure. That is an receptor tyrosine kinase and DCrk can directly bind to the receptor when the receptor is auto-phosphorylated.
We also isolated Drosophila homologs of two major Crk SH2 binding molecules, Paxillin and p130Cas. However, we could not get any evidences suggesting their requirements for Crk signaling pathway during Drosophila development.
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Research Products
(2 results)
