Synergistic Effects of a Chalkophore, Methanobactin, on Microbial Methylation of Mercury.
Synergistic Effects of a Chalkophore, Methanobactin, on Microbial Methylation of Mercury.
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Chalkophore、Methanobactin 对汞的微生物甲基化的协同作用。
DOI：
10.1128/aem.00122-20
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发表时间：
2020
影响因子：
4.4
通讯作者：
Gu Baohua
中科院分区：
文献类型：
--
作者：
Yin Xixiang;Wang Lihong;Zhang Lijie;Chen Hongmei;Liang Xujun;Lu Xia;DiSpirito Alan A;Semrau Jeremy D;Gu Baohua
神经毒素甲基汞（MeHg）的微生物产生是一个重大的健康和环境问题，因为它可以在食物网中进行生物积累和生物放大。一种被称为甲烷菌素（MB）的荧光体或铜结合化合物，已被证明能与汞[作为Hg(II)]形成强配合物，并使一些甲烷氧化菌能够降解甲基汞。然而，目前尚不清楚Hg（II）与MB结合是否也能阻碍Hg（II）被其他微生物甲基化。与预期相反，甲基化菌Methylosinus trichosporium OB3b （OB3b-MB）产生的MB比汞甲基化菌Desulfovibrio脱硫菌ND132和Geobacter sulphreducens PCA所观察到的硫醇化合物（如半胱氨酸）更能提高汞（II）甲基化的速度和效率。与无mb对照相比，OB3b-MB降低了Hg（II）的吸收和内化率，但使甲基化率提高了5- 7倍，这表明与OB3b-MB的Hg（II）络合促进了甲基化所需的Hg（II）的交换和内部转移到HgcAB蛋白。相反，添加过量的OB3b-MB或来自methylocystis菌株SB2 （SB2-MB）的不同形式的MB抑制Hg（II）甲基化，可能是由于Hg（II）的结合更大。总之，我们的研究结果强调了微生物外源金属清除化合物在控制环境中甲基汞的净产量和生物积累中的复杂作用。一些厌氧微生物将无机汞（Hg）转化为神经毒素甲基汞，甲基汞可以在食物网中生物积累和生物放大。虽然微生物汞甲基化的遗传基础是已知的，但控制环境中净甲基汞产生的因素仍然知之甚少。在这里，研究表明汞甲基化可以被一些甲烷氧化菌产生的一种形式的外源铜结合化合物（甲烷obactin）大大增强，而另一种形式则不能。这一新发现表明微生物之间存在复杂的相互作用，这些相互作用可能会影响原位甲基汞的净产量。
Microbial production of the neurotoxin methylmercury (MeHg) is a significant health and environmental concern, as it can bioaccumulate and biomagnify in the food web. A chalkophore or a copper-binding compound, termed methanobactin (MB), has been shown to form strong complexes with mercury [as Hg(II)] and also enables some methanotrophs to degrade MeHg. It is unknown, however, if Hg(II) binding with MB can also impede Hg(II) methylation by other microbes. Contrary to expectations, MB produced by the methanotroph Methylosinus trichosporium OB3b (OB3b-MB) enhanced the rate and efficiency of Hg(II) methylation more than that observed with thiol compounds (such as cysteine) by the mercury-methylating bacteria Desulfovibrio desulfuricans ND132 and Geobacter sulfurreducens PCA. Compared to no-MB controls, OB3b-MB decreased the rates of Hg(II) sorption and internalization, but increased methylation by 5- to 7-fold, suggesting that Hg(II) complexation with OB3b-MB facilitated exchange and internal transfer of Hg(II) to the HgcAB proteins required for methylation. Conversely, addition of excess amounts of OB3b-MB or a different form of MB fromMethylocystisstrain SB2 (SB2-MB) inhibited Hg(II) methylation, likely due to greater binding of Hg(II). Collectively, our results underscore the complex roles of microbial exogenous metal-scavenging compounds in controlling net production and bioaccumulation of MeHg in the environment.IMPORTANCESome anaerobic microorganisms convert inorganic mercury (Hg) into the neurotoxin methylmercury, which can bioaccumulate and biomagnify in the food web. While the genetic basis of microbial mercury methylation is known, factors that control net methylmercury production in the environment are still poorly understood. Here, it is shown that mercury methylation can be substantially enhanced by one form of an exogenous copper-binding compound (methanobactin) produced by some methanotrophs, but not by another. This novel finding illustrates that complex interactions exist between microbes and that these interactions can potentially affect the net production of methylmercuryin situ.