Chiang C S, Xu Y C, Bremer H
Biology Programs, University of Texas at Dallas, Richardson 75080.
Mol Gen Genet. 1991 Mar;225(3):435-42. doi: 10.1007/BF00261684.
The in vivo role of the Escherichia coli protein DnaA in the replication of plasmid pBR322 was investigated, using a plasmid derivative carrying an inducible dnaA+ gene. In LB medium without inducer, the replication of this plasmid, like that of pBR322, was inhibited by heat inactivation of chromosomal DnaA46 protein so that plasmid accumulation ceased 1 to 2 h after the temperature shift. This inhibition did not occur when the plasmid dnaA+ gene was expressed in the presence of the inducer isopropyl-1-thio-beta-D-galactopyranoside (IPTG). Inhibition was also not observed in glycerol minimal medium or in the presence of low concentrations of rifampicin or chloramphenicol. Deletion of the DnaA binding site and the primosome assembly sites (pas, rri) downstream of the replication origin did not affect the plasmid copy number during exponential growth at 30 degrees C, or after inactivation of DnaA by a shift to 42 degrees C in a dnaA46 host, or after oversupply of DnaA, indicating that these sites are not involved in a rate-limiting step for replication in vivo. The accumulation of the replication inhibitor, RNAI, was independent of DnaA activity, ruling out the possibility that DnaA acts as a repressor of RNAI synthesis, as has been suggested in the literature. Changes in the rate of plasmid replication in response to changes in DnaA activity (in LB medium) could be resolved into an early, rom-dependent, and a late, rom-independent component. Rom- plasmids show only the late effect. After heat inactivation of DnaC, plasmid replication ceased immediately.(ABSTRACT TRUNCATED AT 250 WORDS)
利用携带可诱导dnaA⁺基因的质粒衍生物,研究了大肠杆菌蛋白DnaA在质粒pBR322复制中的体内作用。在没有诱导剂的LB培养基中,该质粒的复制,如同pBR322的复制一样,会因染色体DnaA46蛋白的热失活而受到抑制,以至于在温度转变后1至2小时质粒积累停止。当质粒dnaA⁺基因在诱导剂异丙基-1-硫代-β-D-吡喃半乳糖苷(IPTG)存在下表达时,这种抑制作用不会发生。在甘油基本培养基中或在低浓度利福平或氯霉素存在下也未观察到抑制作用。删除复制起点下游的DnaA结合位点和引发体组装位点(pas、rri),在30℃指数生长期间、在dnaA46宿主中通过转移至42℃使DnaA失活后或在DnaA供应过量后,均不影响质粒拷贝数,这表明这些位点不参与体内复制的限速步骤。复制抑制剂RNAI的积累与DnaA活性无关,排除了如文献中所提出的DnaA作为RNAI合成阻遏物的可能性。响应DnaA活性变化(在LB培养基中)时质粒复制速率的变化可分解为早期的、依赖rom的和晚期的、不依赖rom的成分。rom⁻质粒仅表现出晚期效应。DnaC热失活后,质粒复制立即停止。(摘要截短于250字)