Plasmid partition system of the P1par family from the pWR100 virulence plasmid of Shigella flexneri.
Plasmid partition system of the P1par family from the pWR100 virulence plasmid of Shigella flexneri.
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来自福氏志贺氏菌 pWR100 毒力质粒的 P1par 家族的质粒分配系统。
DOI：
10.1128/jb.187.10.3369-3373.2005
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发表时间：
2005
影响因子：
3.2
通讯作者：
Austin,Stuart
中科院分区：
文献类型：
--
作者：
Sergueev,Kirill;Dabrazhynetskaya,Alena;Austin,Stuart
P1 par家族成员促进革兰氏阴性菌中多种质粒和质粒原噬菌体的主动分离。每一个都有帕拉和ParB蛋白的基因，然后是parS分配位点。福氏志贺菌大毒力质粒pWR 100含有一个新的P1 par家族成员：pWR 100 par。虽然存在典型的parA和parB基因，但推定的pWR 100 parS位点在序列和组织上是非典型的。而pWR 100 parS在大肠杆菌中的质粒分配准确率较高。独特的BoxB六聚体基序在部分内定义了先前描述的家族成员之间的物种特异性。虽然与E. coli，pWR 100 parS具有相同的BoxB序列。正如预测的那样，这两种类型的物种特异性证明是相同的。它们也共享分区介导的不相容性，与不相容性和物种特异性之间的机制联系一致。在pWR 100 parS和P1 parS之间的几个信息序列差异中，在pWR 100 parS位点的中心存在21-bp插入片段。这个插入片段的删除使大部分parS活性保持不变。具有整数螺旋DNA转角的中心插入物的耐受性反映了这些位点的关键拓扑结构，这些位点通过结合宿主IHF蛋白而弯曲。
P1parfamily members promote the active segregation of a variety of plasmids and plasmid prophages in gram-negative bacteria. Each has genes for ParA and ParB proteins, followed by aparSpartition site. The large virulence plasmid pWR100 ofShigella flexnericontains a new P1parfamily member: pWR100par. Although typicalparAandparBgenes are present, the putative pWR100parSsite is atypical in sequence and organization. However, pWR100parSpromoted accurate plasmid partition inEscherichia coliwhen the pWR100 Par proteins were supplied. Unique BoxB hexamer motifs withinparSdefine species specificities among previously described family members. Although substantially different from P1parSfrom the P1 plasmid prophage ofE. coli, pWR100parShas the same BoxB sequence. As predicted, the species specificity of the two types proved identical. They also shared partition-mediated incompatibility, consistent with the proposed mechanistic link between incompatibility and species specificity. Among several informative sequence differences between pWR100parSand P1parSis the presence of a 21-bp insert at the center of the pWR100parSsite. Deletion of this insert left much of theparSactivity intact. Tolerance of central inserts with integral numbers of helical DNA turns reflects the critical topology of these sites, which are bent by binding the host IHF protein.