Sledjeski D, Gottesman S
Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4255.
Proc Natl Acad Sci U S A. 1995 Mar 14;92(6):2003-7. doi: 10.1073/pnas.92.6.2003.
The regulation of capsular polysaccharide synthesis in Escherichia coli K-12 depends on the level of an unstable positive regulator, RcsA. The amount of RcsA protein is limited both by its rapid degradation by Lon, an ATP-dependent protease, and by its low level of synthesis. We have found that the low level of expression from the rcsA promoter is due to transcriptional silencing by the histone-like protein H-NS; this silencing is sensitive to both sequence and context in a region upstream of the -35 region of the promoter. A small (85-nt) RNA, DsrA, when overproduced, activates transcription of rcsA::lacZ fusions by counteracting H-NS silencing. DsrA RNA does not show any extended homology with the rcsA promoter or other sequenced regions of E. coli. Since the stimulation of rcsA transcription by this small RNA does not depend on any sequences from within the rcsA transcript, DsrA acts, either directly or indirectly, on rcsA transcription initiation.
大肠杆菌K-12中荚膜多糖合成的调控取决于一种不稳定的正调控因子RcsA的水平。RcsA蛋白的量受到两种因素的限制,一是被Lon(一种ATP依赖性蛋白酶)快速降解,二是其合成水平较低。我们发现,rcsA启动子的低表达水平是由于类组蛋白H-NS的转录沉默所致;这种沉默对启动子-35区上游区域的序列和上下文都很敏感。一种小(85个核苷酸)RNA,DsrA,过量产生时,通过抵消H-NS沉默来激活rcsA::lacZ融合基因的转录。DsrA RNA与rcsA启动子或大肠杆菌的其他测序区域没有任何广泛的同源性。由于这种小RNA对rcsA转录的刺激不依赖于rcsA转录本内的任何序列,DsrA直接或间接地作用于rcsA转录起始。