Transcriptional Regulation in Yeast Genomic Chromatin
| Project/Area Number |
09044235
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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 |
Molecular biology
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| Research Institution | Meisei University (1998-1999)
Tokyo University of Pharmacy and Life Science (1997) |
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Principal Investigator |
SHIMIZU Mitsuhiro Meisei University, Faculty of Physical Sciences and Engineering, Associate Professor, 理工学部, 助教授 (80231364)
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| Co-Investigator(Kenkyū-buntansha) |
MITCHELL Aar Columbia University, Institute of Cancer, Associate
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | chromatin / nucleosome / histone deacetylation / protein-DNA interaction / transcription / repressor / budding yeast / meiosis / ゲノム / DNA-蛋白質相互作用 / クロマリン |
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| Research Abstract |
The purpose of this project is to elucidate mechanisms of transcriptional regulation through chromatin alteration in early meiotic genes in yeast Saccharomyces cerevisiae. The process of entering meiosis in S. cerevisiae is regulated by both environmental signals and a cascade of regulatory genes. The IME1 and IME2 (Inducer of meiosis) gene products play a pivotal role in the decision to initiate meiosis. Rme1p represses IME1 in haploid cells, which are unable to enter meiosis, whereas Ume6p complexed with histone deacetylase Rpd3p represses IME2 in vegetative cells. In this study, we examined mechanisms of repression by Rme1p and Ume6p-Rpd3p in vivo. We demonstrated that Rme1p acts at a distance to prevent activators from binding to their target sites to exert repression in vivo, and proposed that Rme1p may establish a localized repressive chromatin domain. On the other hand, it was shown that activators is present their target sites in promoters repressed by Ume6p-Rpd3p. These results can not be explained by a model proposed widely that histone acetylation-deacetylation modulates the nucleosome structure to regulate trans-acting factor binding. Furthermore, we found that an artificial recruitment of TBP (TATA box binding protein) bypasses repression by Ume6p-Rpd3p, suggesting that histone deacetylarion inhibits TBP binding and/or recruitment of RNA polymerase II holoenzyme. In summery, we proposed novel mechanisms for repression by Rme1p and Ume6p-Rpd3p in relation to chromatin. These findings may be relevant for all eukaryotic cells, since transcription factors studied here are evolutionarily conserved.
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Report
(4 results)
Research Products
(14 results)
