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crp操纵子的自身调控机制:由一个反向RNA转录本进行转录抑制

Mechanism for the autogenous control of the crp operon: transcriptional inhibition by a divergent RNA transcript.

作者信息

Okamoto K, Freundlich M

出版信息

Proc Natl Acad Sci U S A. 1986 Jul;83(14):5000-4. doi: 10.1073/pnas.83.14.5000.

DOI:10.1073/pnas.83.14.5000
PMID:2425359
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC323877/
Abstract

Expression of the crp gene is negatively autoregulated by the complex of cyclic AMP and its receptor protein (cAMP-CRP). We find a second promoter in this region that is strongly activated in vitro and in vivo by cAMP-CRP. Transcription from this promoter is initiated 3 nucleotides upstream and on the opposite strand from the start of crp mRNA. The addition of the purified 5' segment of the divergent RNA specifically inhibits crp transcription in vitro. cAMP-CRP does not block crp expression if the new promoter is altered so that divergent RNA cannot be made. The initial nucleotides of the divergent RNA are complementary to 10 of the first 11 nucleotides of the crp mRNA. Since the next 11 nucleotides of crp mRNA are A + U-rich, and RNA hybrid between the divergent RNA and the 5' end of crp mRNA could produce a structure similar to a rho-independent terminator, leading to inhibition of crp transcription.

摘要

环磷腺苷(cAMP)与其受体蛋白(cAMP-CRP)的复合物对crp基因的表达进行负向自我调节。我们在该区域发现了第二个启动子,其在体外和体内均被cAMP-CRP强烈激活。该启动子的转录起始于crp mRNA起始位点上游3个核苷酸处,且位于相反链上。添加纯化的分歧RNA的5'片段可在体外特异性抑制crp转录。如果新启动子发生改变,使得无法产生分歧RNA,cAMP-CRP则不会阻断crp表达。分歧RNA的起始核苷酸与crp mRNA前11个核苷酸中的10个互补。由于crp mRNA的接下来11个核苷酸富含A + U,分歧RNA与crp mRNA 5'端之间的RNA杂交可能产生类似于不依赖ρ因子的终止子的结构,从而导致crp转录受到抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/3748b35daca0/pnas00318-0038-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/9ba281eb46b3/pnas00318-0036-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/d5c1a497b8aa/pnas00318-0036-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/a7bd4aa15983/pnas00318-0037-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/db06182b42eb/pnas00318-0037-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/ccc7e263d789/pnas00318-0037-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/f463231d3e58/pnas00318-0038-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/6439cc0d4e8b/pnas00318-0038-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/3748b35daca0/pnas00318-0038-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/9ba281eb46b3/pnas00318-0036-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/d5c1a497b8aa/pnas00318-0036-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/a7bd4aa15983/pnas00318-0037-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/db06182b42eb/pnas00318-0037-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/ccc7e263d789/pnas00318-0037-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/f463231d3e58/pnas00318-0038-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/6439cc0d4e8b/pnas00318-0038-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9044/323877/3748b35daca0/pnas00318-0038-c.jpg

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