Effects of the Min system on nucleoid segregation in Escherichia coli

Effects of the Min system on nucleoid segregation in Escherichia coli
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DOI:
10.1099/00221287-148-10-3213
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发表时间:
2002-10-01
期刊:
影响因子:
2.8
通讯作者:
Nordström, K
Nordström, K
中科院分区:
生物学4区
文献类型:
--
作者:
Åkerlund, T;Gullbrand, B;Nordström, K

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大肠杆菌的Min系统通过涉及其所有三种组成蛋白MinC、MinD和MinE的动态定位的机制将细胞分裂引导至中间细胞。Min系统和类核都对细胞分裂有负调控作用,E.缺乏功能性Min系统的大肠杆菌除了在新分离的类核之间的无类核区域外,还可以在无类核细胞极处分裂。有趣的是,E。Min系统有缺陷的大肠杆菌菌株会干扰类核分离,但这种干扰的原因尚不清楚。这里报道了促进极性分裂频率更高的生长条件也导致类核分离更明显的紊乱。在一个完整的Min系统的菌株,表达MinE,但不是MinD,从诱导型启动子受损的类核分离。这些结果表明,在min突变体中的扰动的类核分离不是由极性分裂本身引起的,也不是由染色体二聚体的分辨率受损引起的;在min突变体中,留下了min系统对类核分离有直接影响的可能性。还显示了受干扰的类核分离如何部分地解释了在min突变体群体中明显大多数细胞含有2(n)(n = 0,1,2.)复制的起源
The Min system of Escherichia coli directs cell division to the mid-cell by a mechanism that involves the dynamic localization of all of its three constituent proteins, MinC, MinD and MinE. Both the Min system and the nucleoid regulate cell division negatively and strains of E. coli lacking a functional Min system can divide at nucleoid-free cell poles in addition to the nucleoid-free region between newly segregated nucleoids. Interestingly, E. coli strains with a defective Min system have disturbed nucleoid segregation and the cause for this disturbance is not known. it is reported here that growth conditions promoting a higher frequency of polar divisions also lead to a more pronounced disturbance in nucleoid segregation. In strains with an intact Min system, expression of MinE, but not of MinD, from an inducible promoter was followed by impaired nucleoid segregation. These results suggest that the disturbed nucleoid segregation in min mutants is not caused by polar divisions per se, nor by impaired resolution of chromosome dimers; in min mutants, leaving open the possibility that the Min system has a direct effect on nucleoid segregation. It is also shown how the disturbed nucleoid segregation can explain in part the unexpected finding that the clear majority of cells in min mutant populations contain 2(n) (n = 0, 1, 2...) origins of replication.