Shkilnyj Paul, Koudelka Gerald B
Department of Biological Sciences, University at Buffalo, Cooke Hall, North Campus, Buffalo, NY, USA.
J Bacteriol. 2007 Apr;189(8):3115-23. doi: 10.1128/JB.01857-06. Epub 2007 Feb 16.
The affinities of the bacteriophage 434 repressor for its various binding sites depend on the type and/or concentration of monovalent cations. The ability of bacteriophage 434 repressor to govern the lysis-lysogeny decision depends on the DNA binding activities of the phage's cI repressor protein. We wished to determine whether changes in the intracellular ionic environment influence the lysis-lysogeny decision of the bacteriophage lambda(imm434). Our findings show that the ionic composition within bacterial cells varies with the cation concentration in the growth media. When lambda(imm434) lysogens were grown to mid-log or stationary phase and subsequently incubated in media with increasing monovalent salt concentrations, we observed a salt concentration-dependent increase in the frequency of bacteriophage spontaneous induction. We also found that the frequency of spontaneous induction varied with the type of monovalent cation in the medium. The salt-dependent increase in phage production was unaffected by a recA mutation. These findings indicate that the salt-dependent increase in phage production is not caused by activation of the SOS pathway. Instead, our evidence suggests that salt stress induces this lysogenic bacteriophage by interfering with 434 repressor-DNA interactions. We speculate that the salt-dependent increase in spontaneous induction is due to a direct effect on the repressor's affinity for DNA. Regardless of the precise mechanism, our findings demonstrate that salt stress can regulate the phage lysis-lysogeny switch.
噬菌体434阻遏物对其各种结合位点的亲和力取决于单价阳离子的类型和/或浓度。噬菌体434阻遏物控制裂解-溶原决定的能力取决于噬菌体cI阻遏蛋白的DNA结合活性。我们希望确定细胞内离子环境的变化是否会影响噬菌体λ(imm434)的裂解-溶原决定。我们的研究结果表明,细菌细胞内的离子组成随生长培养基中阳离子浓度的变化而变化。当λ(imm434)溶原菌生长到对数中期或稳定期,随后在单价盐浓度不断增加的培养基中孵育时,我们观察到噬菌体自发诱导频率随盐浓度的增加而增加。我们还发现,自发诱导的频率随培养基中单价阳离子的类型而变化。噬菌体产生的盐依赖性增加不受recA突变的影响。这些发现表明,噬菌体产生的盐依赖性增加不是由SOS途径的激活引起的。相反,我们的证据表明,盐胁迫通过干扰434阻遏物与DNA的相互作用来诱导这种溶原性噬菌体。我们推测,自发诱导的盐依赖性增加是由于对阻遏物与DNA亲和力的直接影响。无论确切机制如何,我们的研究结果表明盐胁迫可以调节噬菌体的裂解-溶原开关。