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, D. desulfuricans ND132 and G. sulfurreducens PCA. Compared to no-MB controls, OB3b-MB decreased the rates of Hg(II) sorption and internalization, but increased methylation by 5–7 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 from Methylocystis strain SB2 (SB2-MB) inhibited Hg(II) methylation, likely due to greater binding of Hg(II). Collectively our results underscore complex roles of exogenous metal-scavenging compounds produced by microbes in controlling net production and bioaccumulation of MeHg in the environment.

IMPORTANCE: Some 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 methylmercury in situ.

微生物产生的神经毒素甲基汞（MeHg）是健康和环境方面的重要问题，因为它可以在食物网中生物累积和生物放大。已经显示了一种被称为甲氧杆菌素（MB）的生粉团或铜结合化合物与汞形成强络合物[以Hg（II）的形式存在]，并且还使一些甲烷营养生物能够降解MeHg。但是，未知的是，Hg（II）与MB的结合是否也可以阻止其他微生物对Hg（II）的甲基化。与预期相反，甲烷氧化菌甲基毛孢菌OB3b（OB3b-MB）产生的MB比汞-甲基化细菌D. desulfuricans对硫醇化合物（如半胱氨酸）所观察到的Hg（II）甲基化速率和效率更高。 ND132和G.sulfreducensPCA。与无MB对照相比，OB3b-MB降低了Hg（II）的吸附和内在化速率，但使甲基化提高了5-7倍，这表明Hg（II）与OB3b-MB的络合促进了Hg（II）的交换和内部转移II）甲基化所需的HgcAB蛋白。相反地，加入过量的OB3b-MB或来自不同形式的MB的Methylocystis应变SB2（SB2-MB）抑制汞（II）的甲基化，可能是由于较大的汞（II）的结合。总的来说，我们的结果强调了微生物产生的外源金属清除化合物在控制环境中MeHg的净产量和生物积累方面的复杂作用。

重要信息：一些厌氧微生物将无机汞（Hg）转化为神经毒素，甲基汞，它们可以在食物网中生物累积和生物放大。尽管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生产的因素仍然知之甚少。在此显示出，汞甲基化可以通过一种由甲烷异养生物产生的外源性铜结合化合物（甲烷杆菌素）的一种形式得到显着增强，而另一种形式则不能。这个新发现说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甲基汞的原位净生产。