Castro-Cerritos Karla Viridiana, Lopez-Torres Adolfo, Obregón-Herrera Armando, Wrobel Katarzyna, Wrobel Kazimierz, Pedraza-Reyes Mario
Division of Natural and Exact Sciences, Department of Biology, University of Guanajuato, Guanajuato, Mexico.
Institute of Applied Chemistry, University of Papaloapan, Tuxtepec, Oaxaca, Mexico.
Curr Genet. 2018 Feb;64(1):215-222. doi: 10.1007/s00294-017-0722-7. Epub 2017 Jun 17.
The non-appropriate conditions faced by nutritionally stressed bacteria propitiate error-prone repair events underlying stationary-phase- or stress-associated mutagenesis (SPM). The genetic and molecular mechanisms involved in SPM have been deeply studied but the biochemical aspects of this process have so far been less explored. Previous evidence showed that under conditions of nutritional stress, non-dividing cells of strain B. subtilis YB955 overexpressing ribonucleotide reductase (RNR) exhibited a strong propensity to generate true reversions in the hisC952 (amber), metB5 (ochre) and leuC425 (missense) mutant alleles. To further advance our knowledge on the metabolic conditions underlying this hypermutagenic phenotype, a high-throughput LC-MS/MS proteomic analysis was performed in non-dividing cells of an amino acid-starved strain, deficient for NrdR, the RNR repressor. Compared with the parental strain, the level of 57 proteins was found to increase and of 80 decreases in the NrdR-deficient strain. The proteomic analysis revealed an altered content in proteins associated with the stringent response, nucleotide metabolism, DNA repair, and cell signaling in amino acid-starved cells of the ∆nrdR strain. Overall, our results revealed that amino acid-starved cells of strain B. subtilis ∆nrdR that escape from growth-limiting conditions exhibit a complex proteomic pattern reminiscent of a disturbed metabolism. Future experiments aimed to understand the consequences of disrupting the cell signaling pathways unveiled in this study, will advance our knowledge on the genetic adaptations deployed by bacteria to escape from growth-limiting environments.
营养应激细菌所面临的不适宜条件会促使易错修复事件发生,这些事件是静止期或应激相关诱变(SPM)的基础。虽然已经深入研究了参与SPM的遗传和分子机制,但到目前为止,对该过程的生化方面研究较少。先前的证据表明,在营养应激条件下,过表达核糖核苷酸还原酶(RNR)的枯草芽孢杆菌YB955菌株的非分裂细胞在hisC952(琥珀突变)、metB5(赭石突变)和leuC425(错义突变)等位基因中表现出强烈的产生真正回复突变的倾向。为了进一步了解这种高诱变表型背后的代谢条件,我们对缺乏RNR阻遏物NrdR的氨基酸饥饿菌株的非分裂细胞进行了高通量LC-MS/MS蛋白质组分析。与亲本菌株相比,在缺乏NrdR的菌株中发现57种蛋白质水平升高,80种蛋白质水平降低。蛋白质组分析揭示了在ΔnrdR菌株的氨基酸饥饿细胞中,与严谨反应、核苷酸代谢、DNA修复和细胞信号传导相关的蛋白质含量发生了变化。总体而言,我们的结果表明,枯草芽孢杆菌ΔnrdR菌株中逃脱生长限制条件的氨基酸饥饿细胞表现出一种复杂的蛋白质组模式,让人联想到代谢紊乱。旨在了解本研究中揭示的细胞信号通路被破坏的后果的未来实验,将增进我们对细菌为逃脱生长限制环境而进行的遗传适应的认识。