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鼠伤寒沙门氏菌噬菌体A3和A4的溶原性转变包括O抗原多糖链重复单元鼠李糖的O-乙酰化。

Lysogenic conversion of Salmonella typhimurium bacteriophages A3 and A4 consists of O-acetylation of rhamnose of the repeating unit of the O-antigenic polysaccharide chain.

作者信息

Wollin R, Stocker B A, Lindberg A A

出版信息

J Bacteriol. 1987 Mar;169(3):1003-9. doi: 10.1128/jb.169.3.1003-1009.1987.

Abstract

Lysogenization of Salmonella typhimurium with either of the bacteriophages A3 and A4 results in O-acetylation of the L-rhamnose residues of the O-polysaccharide chain of the lipopolysaccharide of the bacterial cell envelope. The O-acetyl group is found on both O-2 and O-3 of the L-rhamnosyl residues. This lysogenic conversion prevents the adsorption of the A3 and A4 phages and also greatly reduces the rate of adsorption of phage P22 to the O-polysaccharide chain as measured by binding studies with whole bacteria. Isolated lipopolysaccharide from A3- and A4-lysogenized bacteria was also inefficient in inactivating these phages: the concentration required for 50% inactivation was 10,000-fold higher than that for lipopolysaccharide from S. typhimurium not lysogenized by any A phage. Binding of phages A3 and A4 is accompanied by hydrolysis of the alpha-1,3 linkage between rhamnose and galactose in the tetrasaccharide repeating unit of the O-polysaccharide. Phage hydrolysis generates saccharides of various lengths, the majority being dodecasaccharides, i.e., equivalent to three repeating units. It is surmised that O-acetylation of the rhamnosyl residue interferes with phage A3, A4, and P22 infection by preventing binding to and hydrolysis of the O-polysaccharide chain, the initial step in the phage infection cycle. The new O-acetyl-rhamnose entities did not elicit specific antibodies in rabbits in accordance with earlier experiences. The O-acetylation of O-2 and O-3 of rhamnose is a new, hitherto unknown, modification of the O-polysaccharide chain of S. typhimurium.

摘要

用噬菌体A3和A4中的任何一种使鼠伤寒沙门氏菌溶源化,会导致细菌细胞包膜脂多糖O-多糖链的L-鼠李糖残基发生O-乙酰化。在L-鼠李糖基残基的O-2和O-3位均发现有O-乙酰基。这种溶源转变可阻止A3和A4噬菌体的吸附,并且通过对完整细菌的结合研究测定,还能大大降低噬菌体P22吸附到O-多糖链上的速率。从A3和A4溶源化细菌中分离出的脂多糖在使这些噬菌体失活方面也效率低下:50%失活所需的浓度比未被任何A噬菌体溶源化的鼠伤寒沙门氏菌的脂多糖高10000倍。噬菌体A3和A4的结合伴随着O-多糖四糖重复单元中鼠李糖和半乳糖之间α-1,3键的水解。噬菌体水解产生各种长度的糖类,大多数是十二糖,即相当于三个重复单元。据推测,鼠李糖基残基的O-乙酰化通过阻止与O-多糖链的结合和水解(噬菌体感染周期的第一步)来干扰噬菌体A3、A4和P22的感染。根据早期经验,新的O-乙酰基-鼠李糖实体在兔子中未引发特异性抗体。鼠李糖O-2和O-3位的O-乙酰化是鼠伤寒沙门氏菌O-多糖链一种新的、迄今未知的修饰。

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