Zhang Weiwen, Culley David E, Hogan Mike, Vitiritti Luigi, Brockman Fred J
Microbiology Department, Pacific Northwest National Laboratory, 902 Battelle Boulevard, P.O. Box 999, Richland, WA 99352, USA.
Antonie Van Leeuwenhoek. 2006 Jul;90(1):41-55. doi: 10.1007/s10482-006-9059-9. Epub 2006 May 6.
Sulfate-reducing bacteria such as Desulfovibrio vulgaris have developed a set of responses that allow them to survive in hostile environments. To obtain further knowledge of the protective mechanisms employed by D. vulgaris in response to oxidative stress and heat shock, we performed a genome-wide transcriptomic analysis to determine the cellular responses to both stimuli. The results showed that 130 genes were responsive to oxidative stress, while 427 genes were responsive to heat-shock. Functional analyses suggested that the genes regulated were involved in a variety of cellular functions. Amino acid biosynthetic pathways were induced by both oxidative stress and heat shock treatments, while fatty acid metabolism, purine and cofactor biosynthesis were induced by heat shock only. The rubrerythrin gene (rbr) was up-regulated in response to oxidative stress, suggesting an important role for this protein in the oxidative damage resistance response in D. vulgaris. In addition, thioredoxin reductase (trxB) was also responsive to oxidative stress, suggesting that the thiol-specific redox system might also be involved in oxidative protection in this organism. In contrast, the expression of rubredoxin oxidoreductase (rbo), superoxide dismutase (sodB) and catalase (katA) genes were not regulated in response to oxidative stress. Comparison of cellular responses to oxidative stress and heat-shock allowed the identification of 66 genes that showed a similar drastic response to both environmental perturbations, implying that these genes might be part of the general stress response (GSR) network in D. vulgaris. This hypothesis was further supported by the identification of a conserved motif upstream of these stress-responsive genes.
诸如普通脱硫弧菌之类的硫酸盐还原菌已经形成了一套应对机制，使它们能够在恶劣环境中生存。为了进一步了解普通脱硫弧菌应对氧化应激和热休克所采用的保护机制，我们进行了全基因组转录组分析，以确定细胞对这两种刺激的反应。结果表明，有130个基因对氧化应激有反应，而427个基因对热休克有反应。功能分析表明，所调控的基因涉及多种细胞功能。氧化应激和热休克处理均诱导了氨基酸生物合成途径，而脂肪酸代谢、嘌呤和辅因子生物合成仅由热休克诱导。红氧还蛋白基因（rbr）在氧化应激反应中上调，表明该蛋白在普通脱硫弧菌的抗氧化损伤反应中起重要作用。此外，硫氧还蛋白还原酶（trxB）也对氧化应激有反应，表明硫醇特异性氧化还原系统可能也参与了该生物体的氧化保护。相比之下，红氧还蛋白氧化还原酶（rbo）、超氧化物歧化酶（sodB）和过氧化氢酶（katA）基因的表达在氧化应激反应中不受调控。通过比较细胞对氧化应激和热休克的反应，我们鉴定出66个基因对这两种环境扰动均表现出类似的剧烈反应，这意味着这些基因可能是普通脱硫弧菌一般应激反应（GSR）网络的一部分。这些应激反应基因上游保守基序的鉴定进一步支持了这一假设。
