Project/Area Number |
24570061
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Plant molecular biology/Plant physiology
|
Research Institution | Chubu University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
KOJIMA Shoko 中部大学, 応用生物学部, 講師 (10340209)
TAKAHASHI Hiro 千葉大学大学院, 園芸学研究科, 准教授 (30454367)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 植物 / 発生・分化 / 遺伝子 / 発現制御 / マイクロアレイ / エピジェネティック制御 / DNAメチル化 / ケミカルバイオロジー / エピジェネテック制御 |
Outline of Final Research Achievements |
Leaves develop as flat lateral organs from a shoot apical meristem. Initially, a group of cells is patterned along the proximal-distal axis and then the adaxial-abaxial axis is established, which is crucial for further leaf development. Subsequent cell proliferation along the medial-lateral axis results in flat and symmetric leaves. However, molecular mechanisms are still unknown. We reported that the ASYMMETRIC LEAVES1 (AS1)-AS2 complex represses AUXIN RESPONSE FACTOR3 (ARF3) directly and epigenetically, and indirectly represses ARF3 by PTGS. We found that TOP1α was involved in the AS1-AS2 repression of ARF3. Furthermore, bioinformatic analysis and molecular genetic analysis indicated that expression of Kip-related protein5 (KRP5) (CDK inhibitor) was controlled by AS1-AS2 through ARF3 functions. These results suggest that AS1-AS2 represses KRP5 for regulating cell division in the medial-lateral axis, and it might result in formation of flat and symmetric lamina.
|