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首页> 美国卫生研究院文献>Journal of Bacteriology >Cloning and characterization of the region III flagellar operons of the four Shigella subgroups: genetic defects that cause loss of flagella of Shigella boydii and Shigella sonnei.
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Cloning and characterization of the region III flagellar operons of the four Shigella subgroups: genetic defects that cause loss of flagella of Shigella boydii and Shigella sonnei.

机译：四个志贺氏菌亚组的III区鞭毛操纵子的克隆和鉴定：导致博伊氏志贺氏菌和索氏志贺氏菌鞭毛丧失的遗传缺陷。

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To detect genetic defects that might have caused loss of flagella in Shigella boydii and Shigella sonnei, the region III flagellar (fli) operons were cloned from certain strains and analyzed with reference to the restriction maps and genetic maps of Escherichia coli fli operons. S. boydii NCTC9733 (strain C5 in this paper) had the 988-bp internal deletion in the fliF gene that encodes a large substructural protein of the basal body. Two strains (C1 and C8) had deletions of the entire fliF operon, and the remaining three (C3, C4, and C9) differed in the size of the restriction fragments carrying the fliF and fliL operons. Loss of flagella in S. boydii appears to originate in some defect in the fliF operon. S. sonnei IID969 lacked the fliD gene and, in place of it, carried two IS600 elements as inverted repeats. Genes downstream from fliD were not detected in the cloned fragment despite its large size but did appear elsewhere in the chromosome. The fliD gene encodes a cap protein of the flagellar filament, and its deletion results in overexpression of class 3 operons by the increased amount of FliA (sigmaF) caused by the excess export of the anti-sigma factor FlgM. Three other strains also had the fliD deletion, and two of them had another deletion in the fliF-fliG-fliH region. The fliD deletion might be the primary cause of loss of flagella in S. sonnei. The lack of FliF or FliD in each subgroup is discussed in connection with the maintenance of virulence and bacterial growth. We also discuss the process of loss of flagella in relation to transposition of IS elements and alterations of the noncoding region, which were found to be common to at least three subgroups.
机译：为了检测可能导致波氏志贺氏菌和索尼氏志贺氏菌失去鞭毛的遗传缺陷，从某些菌株中克隆了III区鞭毛（fli）操纵子，并参照大肠杆菌fli操纵子的限制性图谱和遗传图谱进行了分析。博伊氏链球菌NCTC9733（本文中的菌株C5）在fliF基因中具有988 bp的内部缺失，该基因编码一个很大的基体亚结构蛋白。两个菌株（C1和C8）缺失了整个fliF操纵子，其余三个菌株（C3，C4和C9）的携带fliF和fliL操纵子的限制性片段大小不同。博伊氏链球菌鞭毛的损失似乎起因于fliF操纵子的某些缺陷。 S. sonnei IID969缺少fliD基因，并且代替了它，带有两个IS600元件作为反向重复序列。尽管fliD下游的基因很大，但在克隆的片段中并未检测到，但确实出现在染色体的其他位置。 fliD基因编码鞭毛细丝的帽状蛋白，其缺失导致3类操纵子的过表达，这是由于抗σ因子FlgM的过量输出引起的FliA（sigmaF）数量增加所致。其他三株也有fliD缺失，其中两株在fliF-fliG-fliH区有另一处缺失。 fliD缺失可能是S. sonnei中鞭毛损失的主要原因。讨论了在每个亚组中缺乏FliF或FliD的问题，涉及维持毒力和细菌生长。我们还讨论了与IS元素的转座和非编码区的改变有关的鞭毛丢失过程，这些过程对于至少三个亚组是常见的。

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