| Project/Area Number |
16K18396
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Neurochemistry/Neuropharmacology
|
|---|
| Research Institution | Kyoto Prefectural University of Medicine |
|---|
Principal Investigator |
Gotoh Hitoshi 京都府立医科大学, 医学(系)研究科(研究院), 助教 (20462202)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
Ono Katsuhiko 京都府立医科大学, 大学院 医学研究科・神経発生生物学, 教授 (30152523)
Nomura Tadashi 京都府立医科大学, 大学院 医学研究科・神経発生生物学, 准教授 (10323007)
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 神経発生 / 大脳皮質 / 発生 / エネルギー代謝 / グリコーゲン / グリコーゲン代謝 / 神経幹細胞 / 神経 / 細胞内代謝 / 代謝 / 終脳 |
|---|
| Outline of Final Research Achievements |
Glycogen is formed from glucose and its metabolism is known to play a role in energy supply. In this study, we focused on Glycogenin (Gyg), which is the core enzyme of glycogen synthesis, and analyzed its role in the brain development. When we examined the expression of the Gyg gene in the cerebral cortex, it was strongly expressed in the neural stem cells. We introduced knockdown construct by in utero electroporation, and found that differentiation and migration of neurons were disturbed. We further established Gyg KO mice using Crispr/Cas9 method. However, Gyg KO mice showed early postnatal lethality and showed similar abnormality in cortical layer formation.
From these observation, it was suggested that the glycogen metabolic pathway is important for the development of the cerebral cortex.
|
