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首页> 外文期刊>Applied and Environmental Microbiology >Effect of the Deletion of qmoABC and the Promoter-Distal Gene Encoding a Hypothetical Protein on Sulfate Reduction in Desulfovibrio vulgaris Hildenborough
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Effect of the Deletion of qmoABC and the Promoter-Distal Gene Encoding a Hypothetical Protein on Sulfate Reduction in Desulfovibrio vulgaris Hildenborough

机译:qmoABC的缺失和编码假设蛋白的启动子-远端基因对寻常型脱硫弧菌希尔登伯勒中硫酸盐还原的影响

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The pathway of electrons required for the reduction of sulfate in sulfate-reducing bacteria (SRB) is not yet fully characterized. In order to determine the role of a transmembrane protein complex suggested to be involved in this process, a deletion in Desulfovibrio vulgaris Hildenborough was created by marker exchange mutagenesis that eliminated four genes putatively encoding the QmoABC complex and a hypothetical protein (DVU0851). The Qmo (quinone-interacting membrane-bound oxidoreductase) complex is proposed to be responsible for transporting electrons to the dissimilatory adenosine-5′-phosphosulfate reductase in SRB. In support of the predicted role of this complex, the deletion mutant was unable to grow using sulfate as its sole electron acceptor with a range of electron donors. To explore a possible role for the hypothetical protein in sulfate reduction, a second mutant was constructed that had lost only the gene that codes for the DVU0851 protein. The second constructed mutant grew with sulfate as the sole electron acceptor; however, there was a lag that was not present with the wild-type or complemented strain. Neither deletion strain was significantly impaired for growth with sulfite or thiosulfate as the terminal electron acceptor. Complementation of the Δ(qmoABC-DVU0851) mutant with all four genes or only the qmoABC genes restored its ability to grow by sulfate respiration. These results confirmed the prediction that the Qmo complex is in the electron pathway for sulfate reduction and revealed that no other transmembrane complex could compensate when Qmo was lacking.
机译:在还原硫酸盐的细菌(SRB)中还原硫酸盐所需的电子途径尚未完全表征。为了确定跨膜蛋白复合物的作用,该蛋白参与了这一过程,通过标记交换诱变在寻常型脱硫弧菌中产生了一个缺失,该缺失消除了四个假定编码QmoABC复合物的基因和一个假定蛋白(DVU0851)。 Qmo(与醌相互作用的膜结合氧化还原酶)复合物被认为负责将电子传输至SRB中的异化5'-磷酸腺苷还原酶。为了支持这种复合物的预测作用,缺失突变体不能使用硫酸盐作为其唯一的具有一系列电子供体的电子受体来生长。为了探索该假设蛋白在硫酸盐还原中的可能作用,构建了第二个突变体,该突变体仅丢失了编码DVU0851蛋白的基因。第二个构建的突变体以硫酸盐为唯一电子受体生长。但是,野生型或互补型菌株不存在滞后现象。以亚硫酸盐或硫代硫酸盐为末端电子受体,两种缺失菌株均未显着损害其生长。与所有四个基因或仅qmoABC基因互补的Δ(qmoABC-DVU0851)突变体通过硫酸盐呼吸恢复了其生长的能力。这些结果证实了Qmo络合物在硫酸盐还原的电子途径中的预测,并揭示了当缺少Qmo时没有其他跨膜络合物可以补偿。

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