2018 Fiscal Year Final Research Report
Effects of abnormal histone methylation on cerebral cortical histogenesis
| Project/Area Number |
16K19693
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Embryonic/Neonatal medicine
|
|---|
| Research Institution | Keio University |
|---|
Principal Investigator |
SAKAGUCHI YURI 慶應義塾大学, 医学部(信濃町), 助教 (40464888)
|
|---|
| Research Collaborator |
TAKAHASHI Takao
MITSUHASHI Takayuki
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Keywords | 神経発生 / 細胞周期 / エピジェネティクス |
|---|
| Outline of Final Research Achievements |
We focused our research on roles of histone methylation on cell cycle kinetics of neuronal progenitor cells (NPCs). In detail, we have attempted to generate transgenic mice that would be capable of decreasing expression levels of NSD1 protein in the NPCs, by combining RNA interference strategy and tetracycline inducible system. NSD1 is a histone methyl transferase, a causative protein for overgrowth syndrome Sotos syndrome. However, we were unable to generate stable and functional transgenic mice lines.
|
| Free Research Field |
医歯薬学
|
| Academic Significance and Societal Importance of the Research Achievements |
近年、知的障害の重要な原因としてエピジェネティックな異常、すなわち遺伝子の塩基配列変化を伴わない遺伝子発現メカニズムの異常が、中枢神経異常を合併する先天奇形症候群の病態メカニズムとして注目されている。事実、塩基配列を調べても異常を検出できない症例が半数以上存在する点が次世代シーケンサーによる研究で明らかになりつつある。本研究はこれら原因不明の病態メカニズムを解明することを目標に実施した。
|
