Xer recombinase and genome integrity in Helicobacter pylori, a pathogen without topoisomerase IV.
Xer recombinase and genome integrity in Helicobacter pylori, a pathogen without topoisomerase IV.
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DOI：
10.1371/journal.pone.0033310
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发表时间：
2012
期刊：
影响因子：
3.7
通讯作者：
Benghezal M
中科院分区：
文献类型：
--
作者：
Debowski AW;Carnoy C;Verbrugghe P;Nilsson HO;Gauntlett JC;Fulurija A;Camilleri T;Berg DE;Marshall BJ;Benghezal M
在模式生物E.在大肠杆菌中，由相关的XerC和XerD重组酶介导的重组与FtsK易位酶在专门的dif位点复合，将二聚体染色体分解成游离单体，以允许在细胞分裂时有效的染色体分离。对幽门螺杆菌（一种生长缓慢的胃病原体）的计算基因组分析仅确定了一个染色体xer基因（xerH）及其同源dif位点（difH）。在这里，我们表明，直接重复的difH位点之间的重组需要XerH，FtsK，但不是XerT，TnPZ转座子相关的重组酶。xerH失活不是致死性的，但导致每个细胞的DNA增加，表明染色体分离有缺陷。该突变体也未能定殖小鼠，更容易受到紫外线和环丙沙星，诱导DNA断裂，从而重组和染色体二聚体形成。xerH失活和过表达均导致DNA分离缺陷，表明Xer重组在复制调控中的作用。除了染色体二聚体分辨率和基于H. pylori感染时，我们推测XerH可能参与了染色体的脱连锁，尽管H.幽门螺旋杆菌的DNA促旋酶和拓扑异构酶III同源物也被考虑。对该系统的进一步分析将有助于对H. pylori，其引起消化性溃疡和胃癌;用于密切相关的、致病性弯曲杆菌属物种;以及用于缺乏拓扑异构酶IV的不相关的缓慢生长的病原体，如结核分枝杆菌。
In the model organism E. coli, recombination mediated by the related XerC and XerD recombinases complexed with the FtsK translocase at specialized dif sites, resolves dimeric chromosomes into free monomers to allow efficient chromosome segregation at cell division. Computational genome analysis of Helicobacter pylori, a slow growing gastric pathogen, identified just one chromosomal xer gene (xerH) and its cognate dif site (difH). Here we show that recombination between directly repeated difH sites requires XerH, FtsK but not XerT, the TnPZ transposon associated recombinase. xerH inactivation was not lethal, but resulted in increased DNA per cell, suggesting defective chromosome segregation. The xerH mutant also failed to colonize mice, and was more susceptible to UV and ciprofloxacin, which induce DNA breakage, and thereby recombination and chromosome dimer formation. xerH inactivation and overexpression each led to a DNA segregation defect, suggesting a role for Xer recombination in regulation of replication. In addition to chromosome dimer resolution and based on the absence of genes for topoisomerase IV (parC, parE) in H. pylori, we speculate that XerH may contribute to chromosome decatenation, although possible involvement of H. pylori's DNA gyrase and topoisomerase III homologue are also considered. Further analyses of this system should contribute to general understanding of and possibly therapy development for H. pylori, which causes peptic ulcers and gastric cancer; for the closely related, diarrheagenic Campylobacter species; and for unrelated slow growing pathogens that lack topoisomerase IV, such as Mycobacterium tuberculosis.
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影响因子：
11.3
作者：
Ambur OH;Davidsen T;Frye SA;Balasingham SV;Lagesen K;Rognes T;Tønjum T
通讯作者：
Tønjum T
影响因子：
3.7
作者：
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通讯作者：
Roten, Claude-Alain
影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
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DOI：
10.1016/j.bbrc.2006.07.017
发表时间：
2006-09-15
影响因子：
3.1
作者：
Aubry, Alexandra;Fisher, L. Mark;Cambau, Ernmanuelle
通讯作者：
Cambau, Ernmanuelle