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Genetic identification of a respiratory arsenate reductase

机译：呼吸道砷酸还原酶的遗传鉴定

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For more than a decade, it has been recognized that arsenate [H2AsO41-; As(V)] can be used by microorganisms as a terminal electron acceptor in anaerobic respiration. Given the toxicity of arsenic, the mechanistic basis of this process is intriguing, as is its evolutionary origin. Here we show that a two-gene cluster (arrAB; arsenate respiratory reduction) in the bacterium Shewanella sp. strain ANA-3 specifically confers respiratory As(V) reductase activity. Mutants with in-frame deletions of either arrA or arrB are incapable of growing on As(V), yet both are able to grow on a wide variety of other electron acceptors as efficiently as the wild-type. Complementation by the wild-type sequence rescues the mutants' ability to respire As(V). arrA is predicted to encode a 95.2-kDa protein with sequence motifs similar to the molybdenum containing enzymes of the dimethyl sulfoxide reductase family. arrB is predicted to encode a 25.7-kDa iron-sulfur protein. arrA and arrB comprise an operon that contains a twin arginine translocation (Tat) motif in ArrA (but not in ArrB) as well as a putative anaerobic transcription factor binding site upstream of arrA, suggesting that the respiratory As(V) reductase is exported to the periplasm via the Tat pathway and under anaerobic transcriptional control. These genes appear to define a new class of reductases that are specific for respiratory As(V) reduction. [References: 30]
机译：十多年来，人们已经认识到砷酸[H2AsO41-; As（V）]可被微生物用作厌氧呼吸中的末端电子受体。考虑到砷的毒性，该过程的机理基础以及它的进化起源都令人着迷。在这里，我们显示了在细菌希瓦氏菌属种中的两个基因簇（arrAB；砷酸盐呼吸减少）。菌株ANA-3特别赋予呼吸系统As（V）还原酶活性。具有arrA或arrB的框内缺失的突变体无法在As（V）上生长，但是两者都能够像野生型一样高效地在多种其他电子受体上生长。野生型序列的补充可以挽救突变体释放As（V）的能力。预计arrA编码的95.2-kDa蛋白的序列基序类似于二甲基亚砜还原酶家族的含钼酶。预计arrB编码25.7 kDa的铁硫蛋白。 arrA和arrB包含一个操纵子，该操纵子在ArrA中包含一个双精氨酸易位（Tat）基序（但在ArrB中不包含）以及arrA上游的一个假定的厌氧转录因子结合位点，表明呼吸道As（V）还原酶被输出到通过Tat途径并在厌氧转录控制下的周质。这些基因似乎定义了一类新的还原酶，其对呼吸道As（V）还原具有特异性。 [参考：30]

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