2019 Fiscal Year Final Research Report
Analysis of the neural network formation in NZF-2/-3 double knock-out mice that exhibit symptoms of arthrogryposis
| Project/Area Number |
26460259
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
General anatomy (including histology/embryology)
|
|---|
| Research Institution | Fujita Health University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
亀山 俊樹 藤田医科大学, 総合医科学研究所, 助教 (60298544)
|
|---|
| Project Period (FY) |
2014-04-01 – 2020-03-31
|
| Keywords | neural zinc finger / myelin / transcription factor / 神経発生 / 神経回路 / 関節拘縮 / 遺伝子破壊マウス / トランスクリプトーム |
|---|
| Outline of Final Research Achievements |
We generated the double knockout mice for gene silencing of NZF-2 and NZF-3, and compared these mice with normal or single knockout mice of NZF-2 or NZF-3 by their histology and gene-expression levels.
As a result, the neurons did not innervate from spinal cord into the diaphragm or the distal portion of the extremities. In cerebral cortex, the bundles of nerve fibers were completely lost. In the genes that have moderately changed expression levels in the double knockout mice compared to wild type mice, we found ones that control alternative splicing. This finding suggests that NZF-2 and NZF-3 may influence alternative splicing patterns of other genes.
|
| Free Research Field |
神経発生生物学、分子細胞生物学
|
| Academic Significance and Societal Importance of the Research Achievements |
本研究で得られた結果は、神経細胞が神経線維を伸ばして情報網をつくる際に、２つの遺伝子NZF-2とNZF-3が協力して必要不可欠な働きをすることを示しています。また、正常マウスと比べて二重変異マウスでは、他の遺伝子の働き方が変化する可能性があります。こうした遺伝子やNZF-2とNZF-3の働きは、再生医療で神経を再生させたり、遺伝子の働き方の変化を検査して神経難病を診断するなどの応用が期待できます。
|
