2015 Fiscal Year Final Research Report
The mechanism of ubiquitination system in collective cell migration.
| Project/Area Number |
25840068
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Cell biology
|
|---|
| Research Institution | Chiba University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Keywords | Mib / p120ctn / Rac1 / 細胞集団移動 / ユビキチン化 |
|---|
| Outline of Final Research Achievements |
We found that the posterior lateral line primordium (pLLP) migration was delayed in mind bomb (mib) mutants. Mib is an E3 ubiquitin ligase and a positive regulator of Notch signal. We also found that Mib could potentially control cell migration via Notch signaling independent pathway.
We showed that Mib interacted with and ubiquitinated p120 catenin (p120ctn), which controls cell migration. It is known that p120ctn overexpression induces activation of Rac1. We found that Mib suppressed p120ctn dependent Rac1 activation. These data indicate that Mib controls cell migration via negative regulation of p120ctn activity.
Finally, we tested the hypothesis that exaggerated p120ctn activity in mib mutant causes the delay in pLLP migration. Morpholino knockdown of p120ctn rescued pLLP migration defects in mib mutants. Taken together, our data suggest that Mib is involved in pLLP migration through ubiquitination of p120ctn.
|
| Free Research Field |
発生生物学
|
