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2014 Fiscal Year Final Research Report

Mechanisms of epigenetic regulation maintained by AS2 in leaf development of Arabidopsis thaliana

Research Project

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Project/Area Number 24570061
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Plant molecular biology/Plant physiology
Research InstitutionChubu University

Principal Investigator

MACHIDA Chiyoko  中部大学, 応用生物学部, 教授 (70314060)

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
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
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.

Free Research Field

生物学

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Published: 2016-06-03  

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