Abstract：
Formic acid (HCOOH) and dihydrogen (H2) are characteristic products of enterobacterial mixed-acid fermentation, with H2 generation increasing in conjunction with a decrease in extracellular pH. Formate and acetyl-CoA are generated by radical-based and coenzyme A-dependent cleavage of pyruvate catalysed by pyruvate formate-lyase (PflB). Formate is also the source of H2, which is generated along with carbon dioxide through the action of the membrane-associated, cytoplasmically-oriented formate hydrogenlyase (FHL-1) complex. Synthesis of the FHL-1 complex is completely dependent on the cytoplasmic accumulation of formate. Consequently, formate determines its own disproportionation into H2 and CO2 by the FHL-1 complex. Cytoplasmic formate levels are controlled by FocA, a pentameric channel that translocates formic acid/formate bidirectionally between the cytoplasm and periplasm. Each protomer of FocA has a narrow hydrophobic pore through which neutral formic acid can pass. Two conserved amino acid residues, a histidine and a threonine, at the center of the pore control directionality of translocation. The histidine residue is essential for pH-dependent influx of formic acid. Studies with the formate analogue hypophosphite and amino acid variants of FocA suggest that the mechanisms of formic acid efflux and influx differ. Indeed, current data suggest, depending on extracellular formate levels, two separate uptake mechanisms exist, both likely contributing to maintain pH homeostasis. Bidirectional formate/formic acid translocation is dependent on PflB and influx requires an active FHL-1 complex. This review describes the coupling of formate and H2 production in enterobacteria.
摘要：
甲酸（HCOOH）和二氢（H2）是肠杆菌混合酸发酵的特征产物，随着细胞外pH的降低，H2的产生增加。甲酸酯和乙酰辅酶A是由丙酮酸甲酸裂解酶（PflB）催化的丙酮酸酯的基于自由基和辅酶A依赖性裂解产生的。甲酸也是H2的来源，它与二氧化碳一起通过膜相关的作用产生，胞质定向甲酸脱氢酶（FHL-1）复合物。FHL-1复合物的合成完全依赖于甲酸的细胞质积累。因此,甲酸盐通过FHL-1复合物确定其自身歧化为H2和CO2。细胞质甲酸水平由FocA控制，在细胞质和周质之间双向转运甲酸/甲酸的五聚体通道。FocA的每个原聚体都具有狭窄的疏水孔，中性甲酸可以通过该孔。两个保守的氨基酸残基，组氨酸和苏氨酸,在易位的孔控制方向性的中心。组氨酸残基对于甲酸的pH依赖性流入是必需的。对甲酸盐类似物次磷酸盐和FocA氨基酸变体的研究表明，甲酸流出和流入的机制有所不同。的确,目前的数据表明，取决于细胞外甲酸水平，存在两种独立的摄取机制，两者都可能有助于维持pH稳态。双向甲酸盐/甲酸易位取决于PflB并且流入需要活性FHL-1复合物。本文综述了肠杆菌中甲酸盐和H2生产的偶联。
