Wu L F, Mandrand-Berthelot M A
Laboratoire de Microbiologie, CNRS, Villeurbanne, France.
Mol Gen Genet. 1987 Aug;209(1):129-34. doi: 10.1007/BF00329847.
Two classes of mutants defective in benzyl viologen-linked formate dehydrogenase (FDH-BV) activity were isolated from Escherichia coli K12. Class I consisted of four mutants which were specifically devoid of FDH-BV activity. Their mutation mapped between the ssb and melA genes at 92 min on the genome, at a site recently designated fdhF by Pecher et al. (1985). The direction of transcription of gene fdhF was found to be counterclockwise on the E. coli chromosome in one Mudl(Aprlac) fusion mutant. Expression of the lac operon in this mutant was induced by formate and repressed by nitrate, nitrite or trimethylamine N-oxide. It was found to be dependent on the positive control exerted by the fdhA, B and C genes, possibly involved in selenium incorporation, and by an hydB gene affecting the formate hydrogenlyase pathway. Class II, represented by one Mudl(Aprlac) mutant, exhibited no FDH-BV activity and a reduced level of hydrogenase activity. The relevant fdv mutation was shown to be located at 58 min and to affect the expression of fdhF.
从大肠杆菌K12中分离出两类在苄基紫精连接的甲酸脱氢酶（FDH - BV）活性方面存在缺陷的突变体。第一类由四个突变体组成，它们特异性地缺乏FDH - BV活性。它们的突变位于基因组上92分钟处的单链结合蛋白（ssb）和蜜二糖酶A（melA）基因之间，在一个最近被佩彻等人（1985年）命名为fdhF的位点。在一个Mudl（Aprlac）融合突变体中发现，fdhF基因在大肠杆菌染色体上的转录方向是逆时针的。该突变体中乳糖操纵子的表达受甲酸诱导，受硝酸盐、亚硝酸盐或三甲胺N - 氧化物抑制。发现它依赖于fdhA、B和C基因（可能参与硒的掺入）以及影响甲酸氢化酶途径的hydB基因所施加的正调控。第二类由一个Mudl（Aprlac）突变体代表，其没有FDH - BV活性且氢化酶活性水平降低。相关的fdv突变位于58分钟处，并且影响fdhF的表达。
