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首页> 外文期刊>Plasmid: An International Journal Devoted to Extrachromosomal Gene Systems >Replication regulation of ColE1-like plasmids in amino acid-starved Escherichia coli.
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Replication regulation of ColE1-like plasmids in amino acid-starved Escherichia coli.

机译：ColE1样质粒在氨基酸匮乏的大肠杆菌中的复制调控。

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Differential replication of various ColE1-type plasmids in stringent (relA+) and relaxed (relA-) strains of Escherichia coli starved for particular amino acids was reported previously. A role for the plasmid-encoded Rom protein in the stringent control of ColE1 replication has also been demonstrated. Here we have studied the efficiency of replication of five ColE1-type plasmids in E. coli relA+ and relA- strains starved for five amino acids to find the differential replication of each plasmid in cells starved for each amino acid. The efficiency of replication was found to be in positive correlation with the homology between nucleotide sequences of particular loops of RNA I or RNA II and anticodon loops of tRNA molecules corresponding to the kind of the amino acid deprived. Efficient plasmid DNA replication was observed under conditions for which we predicted (on the basis of theoretical calculations) relatively strong interactions between tRNA molecules, expected to occur in high concentrations in an uncharged from, and RNA I or RNA II. When the theoretical possibility of the tRNA-RNA I or tRNA-RNA II interactions was very small, the observed plasmid DNA replication was negligible. Replication of ColE1-like plasmids during the stringent response was observed only in the absence of a functional rom gene. We observed plasmid replication in the amino acid-starved pcnB relA double mutant. We propose a model for regulation of ColE1 replication in the amino acid-starved E. coli cells based on interactions between uncharged tRNA molecules and RNA I or RNA II. During starvation for different amino acids, different kinds of uncharged tRNA molecules appear in cells (they are much more abundant, however, in relA- mutants than in relA+ hosts) leading to various efficiencies of replication initiation. The Rom protein may modulate the effect of tRNA(s) by enhancing RNAI-RNA II, but not tRNA-RNA I and tRNA-RNA II, interactions.
机译：先前已经报道了在缺乏特定氨基酸的大肠杆菌的严格（relA +）和松弛（relA-）菌株中各种ColE1型质粒的差异复制。还已经证明了质粒编码的Rom蛋白在严格控制ColE1复制中的作用。在这里，我们研究了在缺少五个氨基酸的大肠杆菌relA +和relA-菌株中五个ColE1型质粒复制的效率，以发现每个质粒在每个氨基酸饥饿的细胞中的差异复制。发现复制的效率与RNA I或RNA II的特定环的核苷酸序列与tRNA分子的反密码子环之间的同源性正相关，tRNA分子的反密码子环对应于被剥夺的氨基酸的种类。在我们预测（基于理论计算）的条件下，可以观察到有效的质粒DNA复制，而tRNA分子之间的相互作用则相对较强，而tRNA分子预计在高浓度下不与RNA I或RNA II发生相互作用。当tRNA-RNA I或tRNA-RNA II相互作用的理论可能性很小时，观察到的质粒DNA复制可忽略不计。仅在不存在功能性rom基因的情况下，才观察到严格应答期间类似ColE1的质粒的复制。我们观察到在缺乏氨基酸的pcnB relA双突变体中的质粒复制。我们提出了一个模型，用于基于不带电荷的tRNA分子与RNA I或RNA II之间的相互作用，调节氨基酸缺乏的大肠杆菌细胞中ColE1复制的过程。在饿死不同氨基酸的过程中，不同种类的不带电荷的tRNA分子会出现在细胞中（但是，相对于relA +宿主，它们在relA-突变体中含量要高得多），从而导致各种复制起始效率。 Rom蛋白可通过增强RNAI-RNA II相互作用来调节tRNA的作用，但不能增强tRNA-RNA I和tRNA-RNA II的相互作用。

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