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首页> 外文期刊>Journal of bacteriology >Functional Analysis of Molybdopterin Biosynthesis in Mycobacteria Identifies a Fused Molybdopterin Synthase in Mycobacterium tuberculosis
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Functional Analysis of Molybdopterin Biosynthesis in Mycobacteria Identifies a Fused Molybdopterin Synthase in Mycobacterium tuberculosis

机译：分枝杆菌中钼蝶呤生物合成的功能分析确定结核分枝杆菌中融合的钼蝶呤合酶。

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Most mycobacterial species possess a full complement of genes for the biosynthesis of molybdenum cofactor (MoCo). However, a distinguishing feature of members of the Mycobacterium tuberculosis complex is their possession of multiple homologs associated with the first two steps of the MoCo biosynthetic pathway. A mutant of M. tuberculosis lacking the moaA1-moaD1 gene cluster and a derivative in which moaD2 was also deleted were significantly impaired for growth in media containing nitrate as a sole nitrogen source, indicating a reduced availability of MoCo to support the assimilatory function of the MoCo-dependent nitrate reductase, NarGHI. However, the double mutant displayed residual respiratory nitrate reductase activity, suggesting that it retains the capacity to produce MoCo. The M. tuberculosis moaD and moaE homologs were further analyzed by expressing these genes in mutant strains of M. smegmatis that lacked one or both of the sole molybdopterin (MPT) synthase-encoding genes, moaD2 and moaE2, and were unable to grow on nitrate, presumably as a result of the loss of MoCo-dependent nitrate assimilatory activity. Expression of M. tuberculosis moaD2 in the M. smegmatis moaD2 mutant and of M. tuberculosis moaE1 or moaE2 in the M. smegmatis moaE2 mutant restored nitrate assimilation, confirming the functionality of these genes in MPT synthesis. Expression of M. tuberculosis moaX also restored MoCo biosynthesis in M. smegmatis mutants lacking moaD2, moaE2, or both, thus identifying MoaX as a fused MPT synthase. By implicating multiple synthase-encoding homologs in MoCo biosynthesis, these results suggest that important cellular functions may be served by their expansion in M. tuberculosis.
机译：大多数分枝杆菌物种拥有用于钼辅助因子（MoCo）生物合成的完整基因。然而，结核分枝杆菌复合体的一个显着特征是它们拥有与MoCo生物合成途径的前两个步骤相关的多个同源物。 M的突变体。缺乏 moaA1-moaD1 基因簇的肺结核和其中也删除了 moaD2 的衍生物，在含有硝酸盐作为唯一氮源的培养基中的生长受到严重损害，表明MoCo支持MoCo依赖性硝酸盐还原酶NarGHI的同化功能的可用性降低。但是，该双突变体显示出残留的呼吸硝酸盐还原酶活性，表明它保留了产生MoCo的能力。 M。通过在 M突变株中表达这些基因，进一步分析了结核moaD 和 moaE 同源物。缺少一个或两个唯一的钼蝶呤（MPT）合酶编码基因 moaD2 和 moaE2 的阴茎包膜炎，不能在硝酸盐上生长，大概是因为MoCo依赖性硝酸盐同化活性丧失的结果。 M的表达。 M.中的结核性moaD2 。 smegmatis moaD2 突变体和 M。 M中的结核moaE1 或 moaE2 。 smegmatis moaE2 突变体恢复了硝酸盐同化作用，证实了这些基因在MPT合成中的功能。 M表达。结核moaX 还恢复了 M中MoCo的生物合成。缺少 moaD2 ， moaE2 或两者缺少的耻垢突变体，因此将MoaX鉴定为融合的MPT合酶。通过在MoCo生物合成中牵涉多个合成酶编码同源物，这些结果表明重要的细胞功能可能因其在 M中的扩增而发​​挥作用。结核病。

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