Mizushima T, Ohtsuka Y, Mori H, Miki T, Sekimizu K
Dept. of Microbiology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Mol Gen Genet. 1996 Dec 13;253(3):297-302. doi: 10.1007/pl00008596.
We report here that in Escherichia coli, the anti-bacterial agent nalidixic acid induces transient stabilization and increased synthesis of sigma 32, accompanied by the induction of heat shock proteins (Dnak and GroEL proteins). The induction of heat shock proteins, increased synthesis of sigma 32, and stabilization of sigma 32 observed on treatment of wild-type cells with nalidixic acid were not observed in a nalA26 mutant, a strain that is resistant to nalidixic acid as the result of a mutation in the gyrA gene. Not only oxolinic acid, but also novobiocin, whose targets are the A and B subunits of DNA gyrase, respectively, also induced stabilization and increased synthesis of sigma 32. Thus, inhibition of the activity of DNA gyrase may cause stabilization and increased synthesis of sigma 32, resulting in turn in induction of heat shock proteins.
我们在此报告，在大肠杆菌中，抗菌剂萘啶酸可诱导σ32的短暂稳定和合成增加，同时伴随热休克蛋白（Dnak和GroEL蛋白）的诱导。在用萘啶酸处理野生型细胞时观察到的热休克蛋白诱导、σ32合成增加以及σ32稳定，在nalA26突变体中未观察到，该菌株由于gyrA基因突变而对萘啶酸具有抗性。不仅恶喹酸，而且分别以DNA回旋酶的A和B亚基为靶点的新生霉素，也诱导了σ32的稳定和合成增加。因此，抑制DNA回旋酶的活性可能导致σ32的稳定和合成增加，进而导致热休克蛋白的诱导。
