Chromosome I controls chromosome II replication in Vibrio cholerae.

Chromosome I controls chromosome II replication in Vibrio cholerae.
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DOI:
10.1371/journal.pgen.1004184
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发表时间:
2014-02
期刊:
影响因子:
4.5
通讯作者:
Chattoraj DK
Chattoraj DK
中科院分区:
生物学2区
文献类型:
--
作者:
Baek JH;Chattoraj DK

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染色体复制的控制涉及真核生物中常见的一组调节因子,而具有分裂基因组的细菌使用染色体特异性调节因子。细菌的染色体如何进行复制还不清楚。在霍乱弧菌中,它有两条染色体(chrI和chrII),复制起始由chrI中的DnaA和chrII中的RctB控制。DnaA在chrI复制起点处以及起点之外都有结合位点。RctB同样在chrII起点结合,如图所示,与外部位点结合。与chrII外部位点的结合抑制chrII复制。在chrI中发现了一种新型位点,可以增强chrII的复制。与其增强活性一致,chrI位点增加了RctB与刺激复制的chrII起始位点的结合,并减少了与抑制复制的其他位点的结合。对结合的差异效应表明新位点重塑RctB。该位点的伴侣样活性得到以下发现的支持:它可以减轻chrII复制对伴侣蛋白DnaJ和DnaK的依赖。chrI中存在一个专门控制chrII复制的位点,这表明两条染色体之间存在一种复制通讯机制。分裂细胞中的基因组维持需要染色体在每个细胞周期可靠地复制一次,并且这种复制被定时以允许在细胞分裂之前正确分离子染色体。在基因组分裂的生物体中,真核生物和一类重要的细菌,染色体必须避免相互干扰。它们表现出有纪律的染色体编排,涉及几个调节器和控制电路,即使在最简单的生物体中,也知之甚少。在这里,我们研究的监管过程中参与维持两个染色体的充分研究和医学上重要的病原体霍乱弧菌。我们提供的证据表明,一个网站在染色体I可以控制的频率和时间复制的染色体II。该机制涉及DNA介导的I号染色体位点对II号染色体特异性复制启动子的重塑。该位点通过差异影响其对染色体II上的抑制性和刺激性位点的亲和力来增强蛋白质的活性。我们的研究结果提供了基础,以确定是否协调复制可能是一个保守的功能,保持染色体在增殖细胞的高等生物。
Control of chromosome replication involves a common set of regulators in eukaryotes, whereas bacteria with divided genomes use chromosome-specific regulators. How bacterial chromosomes might communicate for replication is not known. In Vibrio cholerae, which has two chromosomes (chrI and chrII), replication initiation is controlled by DnaA in chrI and by RctB in chrII. DnaA has binding sites at the chrI origin of replication as well as outside the origin. RctB likewise binds at the chrII origin and, as shown here, to external sites. The binding to the external sites in chrII inhibits chrII replication. A new kind of site was found in chrI that enhances chrII replication. Consistent with its enhancing activity, the chrI site increased RctB binding to those chrII origin sites that stimulate replication and decreased binding to other sites that inhibit replication. The differential effect on binding suggests that the new site remodels RctB. The chaperone-like activity of the site is supported by the finding that it could relieve the dependence of chrII replication on chaperone proteins DnaJ and DnaK. The presence of a site in chrI that specifically controls chrII replication suggests a mechanism for communication between the two chromosomes for replication. Genome maintenance in dividing cells requires that the chromosomes replicate reliably once per cell cycle, and that this replication be timed to allow for proper segregation of the daughter chromosomes before cell division. In organisms with divided genomes, eukaryotes and a significant class of bacteria, the chromosomes must avoid interference with one another. They exhibit disciplined chromosome choreography, involving several regulators and control circuits that, even in the simplest organisms, are poorly understood. Here we examine the regulatory processes involved in maintaining the two chromosomes of the well-studied and medically important pathogen Vibrio cholerae. We provide evidence that a site in chromosome I can control the frequency and timing of replication of chromosome II. The mechanism involves a DNA-mediated remodeling of the chromosome II-specific initiator of replication by the chromosome I site. The site enhances the activity of the protein by differentially affecting its affinity for inhibitory and stimulatory sites on chromosome II. Our results provide the groundwork for determining whether coordination of replication might be a conserved feature that maintains chromosomes in proliferating cells of higher organisms.
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发表时间: 2009-05-15
影响因子: 10.5
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