| Project/Area Number |
16J11619
|
|---|
| Research Category |
Grant-in-Aid for JSPS Fellows
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| Allocation Type | Single-year Grants |
|---|
| Section | 国内 |
|---|
| Research Field |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | Kyoto University |
|---|
Principal Investigator |
川端 ケリー 京都大学, 生命科学研究科, 特別研究員(DC2)
|
|---|
| Project Period (FY) |
2016-04-22 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2017: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2016: ¥700,000 (Direct Cost: ¥700,000)
|
|---|
| Keywords | Purkinje cells / filopodia / MTSS1 / DAAM1 / ARP2/3 / formin / actin / development / dendrites |
|---|
| Outline of Annual Research Achievements |
Using parameters measured from timelapse imaging of MTSS1 knockout Purkinje cells (PCs), I performed a computer simulation to model the effect of increased dendritic protrusion length and observed that the resulting dendritic phenotype was similar to real PCs. I further showed that both MTSS1 and DAAM1 are colocalized at the tips of dendritic protrusions in Purkinje cells. Using TIRF microscopy, I observed that MIM inhibits DAAM1 actin-polymerizing activity, and could also see this negative regulation in cells using SiMS imaging. Induced constitutive active expression of DAAM1 in Purkinje cells resulted in increased filopodia length, similar to our MTSS1 mutant phenotype, suggesting MTSS1 inhibits the activity of DAAM1 in developing dendritic protrusions.
|
| Research Progress Status |
29年度が最終年度であるため、記入しない。
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| Strategy for Future Research Activity |
29年度が最終年度であるため、記入しない。
|
