Babykin M M, Sidoruk K V, Zinchenko V V, Nefedova L N, Cerff R, Shestakov S V
International Biotechnological Center, Lomonosov Moscow State University, Moscow, 119899 Russia.
Genetika. 2003 Jan;39(1):25-32.
The role of the prqR gene in the regulation of the adaptive response of the cyanobacterium Synechocystis sp. PCC6803 to the oxidative stress induced with methyl viologen (MV) was studied. For this, transcription activity of prqR and the genes, which may be involved in the control of resistance to MV, was determined by means of Northern blot hybridization in wild-type cells and in the MV-resistant Prq20 mutant with a mutation located in the DNA-binding domain of the PrqR protein. It was ascertained that the prqR gene is a component of the prqR-prqA operon and down regulates its transcription. In cells of the wild-type strain containing MV, the autorepressor activity of the PrqR protein enhances and transcription of mvrA and sodB genes encoding an respectively assumed transporter protein and iron-containing superoxide dismutase increases. The prqR gene may be involved in the negative, indirect control of transcription of these genes. The Prq20 mutant is characterized by an MV-independent derepression of the prqR-prqA operon and by a slightly increased transcription of mvrA and sodB genes not stimulated by MV. Nevertheless, the expression of mvrA and sodB genes was lower than in wild-type cells after the MV treatment. On the strength of this evidence, it is assumed that the main mechanism underlying for the resistance to MV in the Prq20 mutant is derepression of the prqA gene, the product of which is homologous to multidrug transporters, drug efflux proteins.
研究了prqR基因在蓝藻集胞藻PCC6803对甲基紫精（MV）诱导的氧化应激适应性反应调控中的作用。为此，通过Northern印迹杂交法，在野生型细胞和PrqR蛋白DNA结合域发生突变的抗MV的Prq20突变体中，测定了prqR以及可能参与MV抗性控制的基因的转录活性。确定prqR基因是prqR - prqA操纵子的一个组成部分，并下调其转录。在含有MV的野生型菌株细胞中，PrqR蛋白的自抑制活性增强，编码假定的转运蛋白和含铁超氧化物歧化酶的mvrA和sodB基因的转录增加。prqR基因可能参与这些基因转录的负向间接控制。Prq20突变体的特征是prqR - prqA操纵子的MV非依赖性去阻遏，以及mvrA和sodB基因的转录略有增加，且不受MV刺激。然而，MV处理后，mvrA和sodB基因的表达低于野生型细胞。基于这些证据，推测Prq20突变体对MV抗性的主要机制是prqA基因的去阻遏，其产物与多药转运蛋白、药物外排蛋白同源。
