Atlung T, Hansen F G
J Bacteriol. 1983 Dec;156(3):985-92. doi: 10.1128/jb.156.3.985-992.1983.
The rate of synthesis of tryptophan synthetase was found to be increased by heat inactivation of the dnaA protein in three dnaA mutants temperature sensitive for initiation of DNA replication. The effect of the dnaA mutations was dependent upon the presence of an intact attenuator in the tryptophan operon. The activity of the mutated dnaA protein at the tryptophan attenuator and its activity as initiator for chromosome replication decreased gradually with increasing temperature. Two rpoB mutations that suppress the temperature defect of the dnaA46 mutation in initiation of replication were tested for effects on attenuation in the tryptophan operon. One of the rpoB mutations caused increased transcription termination at the attenuator independent of the dnaA allele, whereas the other mutation had no effect. Expression of the histidine and threonine operons, which are also regulated by attenuation, was unaffected by the dnaA mutations.
在三个对DNA复制起始温度敏感的dnaA突变体中,发现通过热失活dnaA蛋白可提高色氨酸合成酶的合成速率。dnaA突变的影响取决于色氨酸操纵子中完整衰减子的存在。突变的dnaA蛋白在色氨酸衰减子处的活性及其作为染色体复制起始因子的活性随温度升高而逐渐降低。测试了两个抑制dnaA46突变在复制起始时温度缺陷的rpoB突变对色氨酸操纵子衰减的影响。其中一个rpoB突变导致衰减子处转录终止增加,与dnaA等位基因无关,而另一个突变没有影响。组氨酸和苏氨酸操纵子也通过衰减进行调控,其表达不受dnaA突变的影响。