| Project/Area Number |
16208002
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Breeding science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MAGATO Yasuo The University of Tokyo, Graduate School of Agricultural and Life Sciences, Professor, 大学院農学生命科学研究科, 教授 (10143413)
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| Co-Investigator(Kenkyū-buntansha) |
KUSABA Makoto The University of Tokyo, Graduate School of Agricultural and Life Sciences, Associate Professor, 大学院農学生命科学研究科, 助教授 (20370653)
ITOH Jun-ichi The University of Tokyo, Graduate School of Agricultural and Life Sciences, Assistant, 大学院農学生命科学研究科, 助手 (30345186)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥50,050,000 (Direct Cost: ¥38,500,000、Indirect Cost: ¥11,550,000)
Fiscal Year 2006: ¥13,000,000 (Direct Cost: ¥10,000,000、Indirect Cost: ¥3,000,000)
Fiscal Year 2005: ¥16,120,000 (Direct Cost: ¥12,400,000、Indirect Cost: ¥3,720,000)
Fiscal Year 2004: ¥20,930,000 (Direct Cost: ¥16,100,000、Indirect Cost: ¥4,830,000)
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| Keywords | rice / shoot / plastochron / phyllotasxy / dorsoventrality / mutant / shoot apical meristem / SHOOTLESS / 向背軸 |
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| Research Abstract |
This research project aims to obtain basic understandings for designing novel architecture of plants, The architecture of the above ground part of plants is mainly determined by the temporal and spatial arrangement of leaves and branches, which are the product of the shoot apical meristem (SAM). Because branches develop at the axils of leaves, primarily important questions are how leaves are formed from the SAM and how they develop to maturity.
We newly identified flattened shoot meristem (fsm) mutant that frequently died during the early vegetative phase. The SAM of fsm was reduced and eventually consumed by leaf primordia. The FSM gene is estimated to encode a chromatin assembly factor that is involved in the regulation of cell cycle, and is expressed in the G1 phase. Although the fsm showed long cell cycle period, developmental timing of leaves (e.g., plastochron) was not affected.
We cloned the causal gene of adl1 mutant that showed adaxialized leaves. The ADL1 encodes calpain-like c
… More
ysteine protease. Interrestinly, shootless3 (shl3) that lacks apical region of embryo and shows shootless phenotype was revealed to be a strong allele of ADL1. Thus, ADL1 is involved in both the regulation of adaxial-abaxial pattern formation of leaves and the establishment of apical region of embryo.
As for temporal regulation of leaf formation, we analyzed plastochron 2 (pla2) mutant that showed short plastochron and small leaves. The PLA2 encodes a RNA binding protein and is orthologous to maize Terminal ear1 gene. PLA2 is expressed in leaf primordia but not in the SAM. Because pla2 leaves matured precociously, primary function of PLA2 is considered to regulate leaf maturation rate.
The fish bone (fib) mutant exhibits pleiotropic phenotypes including narrow leaves, large lamina joint angle, reduced vascular bundles, dwarfism, reduced numbers of crown and lateral roots and agravitropism. These phenotypes are estimated to be caused by the reduced polar auxin transport. The FIB gene encodes a metabolic enzyme of unknown function. Since Arabidopsis mutants of the homilogs of FIB also showed similar abnormalities and reduced polar auxin transport, FIB would be a novel factor for polar auxin transport in plants. Less
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