| Project/Area Number |
13640644
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
植物生理
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| Research Institution | Nagoya University |
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Principal Investigator |
UEGUCHI Chiharu Nagoya University, Bioscience Center, Associated Professor, 生物分子応答研究センター, 助教授 (20232738)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Cytokinin / Phytohormone / Sensor kinase / Signal Transduction / Shoot / シュート / 文化・成長 |
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| Research Abstract |
We identified a set of structurally related genes, AHK2 3 and 4, each encoding a sensor histidine kinase in Arabidopsis thaliana. We identified a loss-of-function mutation of the AHK4 gene. The mutant exhibited the cytokinin-resistant phenotype not only in inhibition of root growth by cytokinin but also in greening and shoot induction of calli. Moreover, AHK4 expressed in budding yeast showed histidine kinase activity in a manner dependent on the presence of cytokinin. These results strongly suggested that AHK4 is involved in the cytokinin-signaling pathway, as a direct receptor. We then screened and isolated loss-of function mutations of the AHK2 and 3 genes. Two independent alleles of ahk3 mutations exhibited the cytokinin-insensitive phenotype in greening and shoot induction of calli, indicating that AHK3 is also a cytokinin receptor. Although two independent alleles of ahk2 showed normal growth and cytokinin sensitivity, the ahk2/ 3 double mutant exhibited semi-dwarf phenotype in the above-ground tissues. These results suggest that AHK2 and 3 also function as cytokinin receptors and that cytokinins act as positive regulators in cell division activity in vivo.
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