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影响鼠伤寒沙门氏菌脂多糖核心结构的rfaH基因,对于F因子功能的表达也是必需的。

Gene rfaH, which affects lipopolysaccharide core structure in Salmonella typhimurium, is required also for expression of F-factor functions.

作者信息

Sanderson K E, Stocker B A

出版信息

J Bacteriol. 1981 May;146(2):535-41. doi: 10.1128/jb.146.2.535-541.1981.

Abstract

Mutations in gene rfaH of Salmonella typhimurium at 84 units on the linkage map make lipopolysaccharide of chemotypes Ra, Rb2, Rb3, and Rc (A. A. Lindberg and C. G. Hellerqvist, J. Gen. Microbiol, 116:25--32, 1980). F-factor expression in RfaH- strains was reduced in the following properties when compared with RfaH+ strains: transfer of Flac, number of phage f2 infective centers, lysis by and propagation of phages f2 and M13, proportion of cells with visible F-pili, and formation of mating aggregates with F- cells. Inhibition of multiplication of Br60, a female-specific phage, was not reduced in RfaH- Flac strains. Plasmid transfer from RfaH- strains was reduced for Inc groups FI, FII, and T, unaffected for Inc groups beta, I alpha, L, N, P, and W. and increased for Inc group M when compared with plasmid transfer from RfaH+ strains. Reduced F-factor function in RfaH- strains was not due to defective lipopolysaccharide since strains with mutations in other rfa genes were unaffected in plasmid transfer. Gene rfaH appears to be homologous with gene sfrB in Escherichia coli K-12, which maps at the same location, influences F-factor function, and affects synthesis of lipopolysaccharide. The gene product of sfrB has been proposed to be a transcription antiterminator.

摘要

鼠伤寒沙门氏菌连锁图谱上84个单位处的rfaH基因突变会产生化学型Ra、Rb2、Rb3和Rc的脂多糖(A. A. 林德伯格和C. G. 赫勒奎斯特,《普通微生物学杂志》,116:25 - 32,1980)。与RfaH⁺菌株相比,RfaH⁻菌株中F因子的表达在以下特性方面有所降低:Flac的转移、噬菌体f2感染中心的数量、噬菌体f2和M13的裂解及增殖、具有可见F菌毛的细胞比例以及与F⁻细胞形成交配聚集体。RfaH⁻ Flac菌株对雌性特异性噬菌体Br60增殖的抑制作用并未降低。与从RfaH⁺菌株进行的质粒转移相比,RfaH⁻菌株中Inc组FI、FII和T的质粒转移减少,Inc组β、Iα、L、N、P和W不受影响,Inc组M的质粒转移增加。RfaH⁻菌株中F因子功能的降低并非由于脂多糖缺陷,因为其他rfa基因突变的菌株在质粒转移方面未受影响。rfaH基因似乎与大肠杆菌K - 12中的sfrB基因同源,sfrB基因位于相同位置,影响F因子功能并影响脂多糖的合成。有人提出sfrB的基因产物是一种转录抗终止因子。

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