| Project/Area Number |
17570032
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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・分子
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| Research Institution | Nagoya University |
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Principal Investigator |
ITO Masaki Graduate School of Bioagricultural Sciences, Nagoya University, Associate Professor, 大学院生命農学研究科, 助教授 (10242851)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | cell cycle / plant cell / cell proliferation / transcriptional regulation / Arabidopsis thaliana / cytokinesis |
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| Research Abstract |
Myb transcription factors with three repeats in the Myb domain (3R-Myb) are encoded by a relatively small subfamily in the large Myb gene family in plants. We have previously shown that this type of Myb proteins have important roles in regulation of G2/M-phase genes in tobacco. The 3R-Myb proteins in plants can be divided into 3 classes (A-type, B-type and C-type 3R-Myb) based on their primary sequences. The aim of this research was to elucidate the molecular mechanisms of transcriptional regulation by 3R-Myb and to identify novel factors that regulate activities of 3R-Myb proteins.
1. We showed that C-type 3R-Myb proteins act as transcriptional repressors on CYCB1 promoter in tobacco cells.
2. The transactivation potential of NtmybA2, a tobacco A-type 3R-Myb protein, is repressed by a regulatory domain located at its C terminus. Deletion of this domain dramatically enhanced its transactivation activity. Our microarray expriments revealed that overexpression of C-terminally deleted version of NtmybA2 resulted in selective upregulation of many G2/M genes that contain MSA elements. The results allowed a genome-wide identification of potential target genes of transcriptianl regulation by NtmybA2 in tobacco cells.
3. In another approach, we aimed to identify the mutation that enhances the cytokinesis defect caused by T-DNA insertion mutation of myb3r4, an A-type 3R-Myb gene in Arabidopsis thaliana. We found that one such mutation is present in genome of the wild-type Lansberg. We could map its locus within a 400-kb region located in upper arm of chromosome 3. Further mapping of this locus and complementation experiments would allow us to identify the gene that are responsible for enhancing the cytokinesis defect in myb3r4 background.
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