Borst D W, Betley M J
Department of Bacteriology, University of Wisconsin-Madison 53706.
Infect Immun. 1993 Dec;61(12):5421-5. doi: 10.1128/iai.61.12.5421-5425.1993.
The mechanism leading to increased production of staphylococcal enterotoxin type A (SEA) in mutant Staphylococcus aureus FRI722 compared within its wild-type parent strain, FRI100, was examined. Sequence analysis revealed two mutations in the upstream promoter region of FRI722 at nucleotides -28 and +3 with respect to the transcriptional initiation site at An sea translational fusion of the upstream region of FRI722 to the structural gene from FRI100 showed an increase in sea expression by Northern (RNA) analysis and in SEA production by Western (immunoblot) analysis. To independently evaluate the effect of each mutation, site-directed mutagenesis was done and revealed that each mutation was responsible for an increase in SEA production.
研究了突变型金黄色葡萄球菌FRI722与其野生型亲本菌株FRI100相比导致A型葡萄球菌肠毒素(SEA)产量增加的机制。序列分析显示,相对于转录起始位点A,FRI722上游启动子区域在核苷酸-28和+3处有两个突变。将FRI722上游区域与FRI100的结构基因进行sea翻译融合,通过Northern(RNA)分析显示sea表达增加,通过Western(免疫印迹)分析显示SEA产量增加。为了独立评估每个突变的影响,进行了定点诱变,结果表明每个突变都导致SEA产量增加。