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Energetic Consequences of Nitrite Stress in Desulfovibrio vulgaris Hildenborough Inferred from Global Transcriptional Analysis

机译:从全球转录分析推论寻常脱硫弧菌Hildenborough中亚硝酸盐胁迫的能量后果。

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摘要

Many of the proteins that are candidates for bioenergetic pathways involved with sulfate respiration in Desulfovibrio spp. have been studied, but complete pathways and overall cell physiology remain to be resolved for many environmentally relevant conditions. In order to understand the metabolism of these microorganisms under adverse environmental conditions for improved bioremediation efforts, Desulfovibrio vulgaris Hildenborough was used as a model organism to study stress response to nitrite, an important intermediate in the nitrogen cycle. Previous physiological studies demonstrated that growth was inhibited by nitrite and that nitrite reduction was observed to be the primary mechanism of detoxification. Global transcriptional profiling with whole-genome microarrays revealed coordinated cascades of responses to nitrite in pathways of energy metabolism, nitrogen metabolism, oxidative stress response, and iron homeostasis. In agreement with previous observations, nitrite-stressed cells showed a decrease in the expression of genes encoding sulfate reduction functions in addition to respiratory oxidative phosphorylation and ATP synthase activity. Consequently, the stressed cells had decreased expression of the genes encoding ATP-dependent amino acid transporters and proteins involved in translation. Other genes up-regulated in response to nitrite include the genes in the Fur regulon, which is suggested to be involved in iron homeostasis, and genes in the Per regulon, which is predicted to be responsible for oxidative stress response.
机译:许多蛋白质是脱硫弧菌属物种中与硫酸盐呼吸有关的生物能途径的候选者。已经研究了,但是对于许多与环境相关的条件,完整的途径和整体细胞生理学仍然有待解决。为了了解在不利的环境条件下这些微生物的代谢状况,以改善生物修复效果,使用了脱硫脱硫希尔德伯勒(Sisulfovibrio vulgaris Hildenborough)作为模型生物来研究对亚硝酸盐(氮循环中重要的中间体)的胁迫反应。以前的生理研究表明,亚硝酸盐抑制了生长,而亚硝酸盐的减少是排毒的主要机理。全基因组微阵列的全球转录谱揭示了能量代谢,氮代谢,氧化应激反应和铁稳态中对亚硝酸盐的协调级联反应。与以前的观察结果一致,除呼吸氧化磷酸化和ATP合酶活性外,亚硝酸盐胁迫的细胞显示出编码硫酸盐还原功能的基因表达减少。因此,压力细胞降低了编码ATP依赖性氨基酸转运蛋白和参与翻译的蛋白质的基因的表达。响应亚硝酸盐而上调的其他基因包括Fur regulon中的基因(建议与铁稳态有关)和Per regulon中的基因(预计与氧化应激反应有关)。

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