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flaR基因在沙门氏菌鞭毛钩形成中的作用

Role of the flaR gene in flagellar hook formation in Salmonella spp.

作者信息

Suzuki T, Iino T

出版信息

J Bacteriol. 1981 Dec;148(3):973-9. doi: 10.1128/jb.148.3.973-979.1981.

DOI:10.1128/jb.148.3.973-979.1981
PMID:7309683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC216300/
Abstract

Flagellar filaments were reconstituted by polymerization with exogenously supplied flagellin monomers at the tips of normal hooks on Salmonella cells which were missing the filaments because of mutations in either the flaL or flaU gene or the flagellin genes H1 and H2. Reconstitution did not occur at the tips of polyhooks of the flaR mutant cells. Thus, the absence of flagellar filaments in the flaR mutant cells was probably caused by the inability of the polyhooks to work as polymerization nuclei for flagellin. A Phf+ mutant which produced polyhooks with flagellar filaments was isolated from a flaR polyhook mutant. Genetic analysis of the Phf+ mutant showed that it carried an intracistronic suppressor mutation of the original flaR mutation. This result indicated that the flaR gene regulates hook length and initiates flagellin formation.

摘要

鞭毛丝通过在沙门氏菌细胞正常钩尖处与外源提供的鞭毛蛋白单体聚合而重建,这些沙门氏菌细胞由于flaL或flaU基因或鞭毛蛋白基因H1和H2的突变而缺少鞭毛丝。在flaR突变细胞的多钩尖处未发生重建。因此,flaR突变细胞中鞭毛丝的缺失可能是由于多钩无法作为鞭毛蛋白的聚合核发挥作用。从flaR多钩突变体中分离出一个产生带有鞭毛丝的多钩的Phf+突变体。对Phf+突变体的遗传分析表明,它携带原始flaR突变的顺反子内抑制突变。这一结果表明,flaR基因调节钩的长度并启动鞭毛蛋白的形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce20/216300/19f04abb0da8/jbacter00265-0242-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce20/216300/19f04abb0da8/jbacter00265-0242-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ce20/216300/19f04abb0da8/jbacter00265-0242-a.jpg

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