| Project/Area Number |
04454607
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
分子生物学
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| Research Institution | Nagoya University |
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Principal Investigator |
AIBA Hiroji Nagoya Univ., School of Science Dept.Molecular Biology, Professor, 理学部, 教授 (20025662)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1993: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | glucose repression / catabolite repression / cAMP / CRP / autoregulation / crp gene / lactose operon / Escherichis coli / グルコース効果 / 転写調節 / 正の自己制御機構 |
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| Research Abstract |
It was found that glucose lowers the amount of cAMP receptor protein(CRP)inEscherichia coli cells. A correlation exists between CRP and b-galactosidase levels in cells growing under various conditions. When the CRP concentration is reduced by manipulating the crp gene, the b-galactosidase expression decreases in proportion to the concentration of CRP.These findings indicate that the lowered concentration of CRP caused by glucose is one of major factors for catabolite repression. We propose that glucose causes catabolite repression by lowering the intracellular levels of both CRP and cAMP.The molecular mechanism underlying the down-regulation of CRP by glucose was investigated. Replacement of the crp promoter to the bla promoter abolishes mostly the glucose-mediated regulation of crp expression. The disruption of the CRP-binding site II essentially eliminates the down-regulation of the crp expression by glucose. It was concluded that the autoregulatory circuit of the crp gene plays a key role in the down-regulation of CRP by glucose.
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