Yan Zhen, Ferry James G
Department of Biochemistry and Molecular Biology, Pennsylvania State University, State College, PA, United States.
Front Microbiol. 2018 Jun 20;9:1322. doi: 10.3389/fmicb.2018.01322. eCollection 2018.
Reduction of the disulfide of coenzyme M and coenzyme B (CoMS-SCoB) by heterodisulfide reductases (HdrED and HdrABC) is the final step in all methanogenic pathways. Flavin-based electron bifurcation (FBEB) by soluble HdrABC homologs play additional roles in driving essential endergonic reactions at the expense of the exergonic reduction of CoMS-SCoM. In the first step of the CO reduction pathway, HdrABC complexed with hydrogenase or formate dehydrogenase generates reduced ferredoxin (Fdx) for the endergonic reduction of CO coupled to the exergonic reduction of CoMS-SCoB dependent on FBEB of electrons from H or formate. Roles for HdrABC:hydrogenase complexes are also proposed for pathways wherein the methyl group of methanol is reduced to methane with electrons from H. The HdrABC complexes catalyze FBEB-dependent oxidation of H for the endergonic reduction of Fdx driven by the exergonic reduction of CoMS-SCoB. The Fdx supplies electrons for reduction of the methyl group to methane. In H independent pathways, three-fourths of the methyl groups are oxidized producing Fdx and reduced coenzyme F (FH). The FH donates electrons for reduction of the remaining methyl groups to methane requiring transfer of electrons from Fdx to F. HdrA1B1C1 is proposed to catalyze FBEB-dependent oxidation of Fdx for the endergonic reduction of F driven by the exergonic reduction of CoMS-SCoB. In H independent acetotrophic pathways, the methyl group of acetate is reduced to methane with electrons derived from oxidation of the carbonyl group mediated by Fdx. Electron transport involves a membrane-bound complex (Rnf) that oxidizes Fdx and generates a Na gradient driving ATP synthesis. It is postulated that F is reduced by Rnf requiring HdrA2B2C2 catalyzing FBEB-dependent oxidation of FH for the endergonic reduction of Fdx driven by the exergonic reduction of CoMS-SCoB. The Fdx is recycled by Rnf and HdrA2B2C2 thereby conserving energy. The HdrA2B2C2 is also proposed to play a role in Fe(III)-dependent reverse methanogenesis. A flavin-based electron confurcating (FBEC) HdrABC complex is proposed for nitrate-dependent reverse methanogenesis in which the oxidation of CoM-SH/CoB-SH and Fdx is coupled to reduction of F. The FH donates electrons to a membrane complex that generates a proton gradient driving ATP synthesis.
异二硫还原酶（HdrED和HdrABC）将辅酶M和辅酶B的二硫键（CoMS-SCoB）还原是所有产甲烷途径的最后一步。可溶性HdrABC同源物基于黄素的电子分叉（FBEB）在驱动必需的吸能反应中发挥额外作用，代价是CoMS-SCoM的放能还原。在CO还原途径的第一步中，与氢化酶或甲酸脱氢酶复合的HdrABC生成还原型铁氧化还原蛋白（Fdx），用于CO的吸能还原，该还原与依赖于来自H或甲酸的电子的FBEB的CoMS-SCoB的放能还原偶联。还提出了HdrABC:氢化酶复合物在甲醇甲基利用来自H的电子还原为甲烷的途径中的作用。HdrABC复合物催化依赖于FBEB的H氧化，用于由CoMS-SCoB的放能还原驱动的Fdx的吸能还原。Fdx为甲基还原为甲烷提供电子。在不依赖H的途径中，四分之三的甲基被氧化生成Fdx和还原型辅酶F（FH）。FH为将剩余甲基还原为甲烷提供电子，这需要电子从Fdx转移到F。有人提出HdrA1B1C催化依赖于FBEB的Fdx氧化，用于由CoMS-SCoB的放能还原驱动的F的吸能还原。在不依赖H的乙酸营养型途径中，乙酸的甲基利用由Fdx介导的羰基氧化产生的电子还原为甲烷。电子传递涉及一种膜结合复合物（Rnf），它氧化Fdx并产生驱动ATP合成的Na梯度。据推测，F被Rnf还原，这需要HdrA2B2C2催化依赖于FBEB的FH氧化，用于由CoMS-SCoB的放能还原驱动的Fdx的吸能还原。Fdx由Rnf和HdrA2B2C2循环利用，从而节约能量。还提出HdrA2B2C2在依赖Fe(III)的反向产甲烷过程中发挥作用。有人提出一种基于黄素的电子分叉（FBEC）HdrABC复合物用于依赖硝酸盐的反向产甲烷过程，其中CoM-SH/CoB-SH和Fdx的氧化与F的还原偶联。FH将电子提供给一个产生驱动ATP合成的质子梯度的膜复合物。
