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Mediators for Activation of fushi tarazu Gene Transcription by BmFTZ-F1
https://ir.soken.ac.jp/records/895
https://ir.soken.ac.jp/records/8956bc816cf-4586-47ee-9ae2-1766dcfe53c3
| 名前 / ファイル | ライセンス | アクション |
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要旨・審査要旨 / Abstract, Screening Result (195.3 kB)
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本文 (1.8 MB)
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| Item type | 学位論文 / Thesis or Dissertation(1) | |||||
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| 公開日 | 2010-02-22 | |||||
| タイトル | ||||||
| タイトル | Mediators for Activation of fushi tarazu Gene Transcription by BmFTZ-F1 | |||||
| タイトル | ||||||
| タイトル | Mediators for Activation of fushi tarazu Gene Transcription by BmFTZ-F1 | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_46ec | |||||
| 資源タイプ | thesis | |||||
| 著者名 |
李, 豊倩
× 李, 豊倩 |
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| フリガナ |
リ, ホウセイ
× リ, ホウセイ |
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| 著者 |
LI, Feng-Qian
× LI, Feng-Qian |
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| 学位授与機関 | ||||||
| 学位授与機関名 | 総合研究大学院大学 | |||||
| 学位名 | ||||||
| 学位名 | 博士（理学） | |||||
| 学位記番号 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 総研大甲第89号 | |||||
| 研究科 | ||||||
| 値 | 生命科学研究科 | |||||
| 専攻 | ||||||
| 値 | 18 遺伝学専攻 | |||||
| 学位授与年月日 | ||||||
| 学位授与年月日 | 1994-03-24 | |||||
| 学位授与年度 | ||||||
| 値 | 1993 | |||||
| 要旨 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | FTZ-FI has been identified as a sequence specific DNA-binding<br /> protein in <i>Drosophila</i>. It binds to a 9 base pairs sequence in the upstream<br /> regulatory region of the <i>fushi tarazu (ftz)</i> gene. Binding site-dependent<br /> expression of the <i>ftz-lacZ</i> fusion genes in transformed embryos showed<br /> that FTZ-F1 is a positive regulator of the <i>ftz</i> gene. A posterior silk gland<br /> extract from the silkworm <i>Bombyx mori</i> contains a factor termed<br /> BmFTZ-F1 which recognizes the same DNA sequence as FTZ-F1 and<br /> has many biochemical characters similar to FTZ-F1. Molecular cloning<br /> of cDNAs for FTZ-F1 and BmFTZ-F1 revealed that they are members of<br /> the steroid hormone receptor superfamily and share homologies in the<br /> DNA-binding and the putative ligand-binding domains. <br /> Using the <i>in vitro</i> transcription systems from posterior silk gland<br /> cells, I found that BmFTZ-F1 can activate transcription of the <i>ftz</i> gene<br /> in a FTZ-F1-binding site dependent manner. To elucidate the mechanism<br /> of transactivation by BmFTZ-F1, I used <i>in vitro</i> transcription systems<br /> from HeLa cells. Because the HeLa system does not contain a FTZ-F1 like<br /> activity, it serves as a recipient in complementation assay for active<br /> components derived from the posterior silk gland extract. The results of<br /> these analyses suggest that two proteins (18kDa and 22kDa polypeptides)<br /> termed MBF (<i>m</i>ediator of BmFTZ-F1) 1 and MBF2, respectively, that<br /> form a heterodimer and mediate activiation of <i>in vitro</i> transcription<br /> from the <i>ftz</i> gene promotor by BmFTZ-F1. Neither MBF1 nor MBF2<br /> binds to DNA. MBF1 interacts with BmFTZ-F1 and stabilizes the<br /> BmFTZ-F1･DNA complex. MBF1 also makes a direct contact with<br /> TATA-binding protein (TBP). Both MBF1 and MBF2 are necessary to<br /> form a complex between BmFTZ-F1 and TBP. I propose a model in<br /> which MBF1 and MBF2 form a bridge between BmFTZ-F1 and TBP,<br /> and mediate transactivation by stabilizing the protein･DNA interactions.<br /> This is the first isolation of mediators capable of modulating transactivator<br /> function directly. | |||||
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| 値 | 有 | |||||
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| 内容記述タイプ | Other | |||||
| 内容記述 | application/pdf | |||||
