Wu J, Weiss B
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.
J Bacteriol. 1992 Jun;174(12):3915-20. doi: 10.1128/jb.174.12.3915-3920.1992.
soxR and soxS are adjacent genes that govern a superoxide response regulon. Previous studies revealed that induction of the regulon is accompanied by increased transcription of soxS, which can activate the target genes. Therefore, induction may occur in two stages: the soxR-dependent activation of soxS, followed by the soxS-dependent induction of other genes. However, the requirement for soxR was unproven because the only existing soxR mutations either were of the regulon-constitutive type or also involved soxS. Therefore, we produced an insertion mutation that was shown by complementation to inactivate only soxR. In confirmation of the two-stage model, soxR was required for the induction by paraquat of the target genes studied (nfo, zwf, and sodA), for paraquat resistance, and for the 47- to 76-fold induction of soxS-lacZ gene fusions. Paraquat did not affect the expression of soxR-lacZ gene fusions. In a soxRS deletion mutant, the regulon was constitutively activated by a runaway soxS+ plasmid. However, a lower-copy-number plasmid failed to activate nfo, zwf, or sodA but did increase the paraquat resistance of a soxRS mutant. Therefore, there is a differential response of the regulon genes to soxS overproduction. A soxR regulon-constitutive mutation was suppressed by a soxR+ plasmid, suggesting a competition between native and activated forms of SoxR. It is proposed that to enhance the sensitivity of the response, the cell minimizes such potential competition by manufacturing only a small amount of this sensor protein, thereby necessitating signal amplification via induction of soxS.
soxR和soxS是相邻基因,它们调控一个超氧化物应答调节子。先前的研究表明,该调节子的诱导伴随着soxS转录的增加,soxS可激活靶基因。因此,诱导可能分两个阶段发生:soxR依赖性激活soxS,随后是soxS依赖性诱导其他基因。然而,soxR的必要性尚未得到证实,因为仅有的现有soxR突变要么是调节子组成型类型,要么也涉及soxS。因此,我们产生了一个插入突变,通过互补试验表明该突变仅使soxR失活。为证实两阶段模型,百草枯诱导所研究的靶基因(nfo、zwf和sodA)、百草枯抗性以及soxS-lacZ基因融合体47至76倍的诱导均需要soxR。百草枯不影响soxR-lacZ基因融合体的表达。在soxRS缺失突变体中,一个失控的soxS+质粒组成型激活该调节子。然而,一个低拷贝数的质粒未能激活nfo、zwf或sodA,但确实增加了soxRS突变体的百草枯抗性。因此,调节子基因对soxS过量表达存在差异反应。一个soxR调节子组成型突变被一个soxR+质粒抑制,这表明SoxR的天然形式和激活形式之间存在竞争。有人提出,为提高应答的敏感性,细胞通过仅制造少量这种传感蛋白来最小化这种潜在竞争,从而需要通过诱导soxS进行信号放大。