| Project/Area Number |
25840081
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Cell biology
|
|---|
| Research Institution | Tokyo Metropolitan Institute of Medical Science |
|---|
Principal Investigator |
YAMAZAKI Satoshi 公益財団法人東京都医学総合研究所, ゲノム医科学研究分野, 研究員 (30648548)
|
|---|
| Research Collaborator |
GILBERT David M. フロリダ州立大学, 教授
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | DNA replication timing / Rif1 / transcription / 転写制御 / DNA replication / Chromatin structure |
|---|
| Outline of Final Research Achievements |
Rif1 is a regulator of replication timing which regulates chromatin loop sizes by binding to nuclear insoluble structures. Depleted of Rif1, but not that of other chromatin factors including cohesion subunits or LaminB1, results in major changes of replication domains in HeLa cells, suggesting that Rif1 is rather unique in its ability to affect genome-wide replication timing. We have analyzed functions of Rif1 using conditional KO mice and cells. Consistent with previous reports in B cells, IgG1 production by class switch recombination is reduced by Rif1 deficiency. We also found a ~1Mb genome segment containing a gene cluster whose transcription is coordinately suppressed by Rif1. This result is consistent with a possibility that Rif1 regulates replication and transcription as well as other chromosome transactions through generation of functional chromatin domains.
|
