Wissenbach U, Ternes D, Unden G
Institut für Biochemie, Heinrich Heine-Universität, Düsseldorf, Federal Republik of Germany.
Arch Microbiol. 1992;158(1):68-73. doi: 10.1007/BF00249068.
The mutant strain AN70 (ubiE) of Escherichia coli which is known to lack ubiquinone (Young IG et al. 1971), was analyzed for menaquinone (MK) and demethylmenaquinone (DMK) contents. In contrast to the wild-type, strain AN70 contained only DMK, but no MK. The mutant strain was able to grow with fumarate, trimethylamine N-oxide (TMAO) and dimethylsulfoxide (DMSO), but not with nitrate as electron acceptor. The membranes catalyzed anaerobic respiration with fumarate and TMAO at 69 and 74% of wild-type rates. DMSO respiration was reduced to 38% of wild-type activities and nitrate respiration was missing (less than or equal to 8% of wild-type), although the respective enzymes were present in wild-type rates. The results complement earlier findings which demonstrated a role for DMK only in TMAO respiration (Wissenbach et al. 1990). It is concluded, that DMK (in addition to MK) can serve as a redox mediator in fumarate, TMAO and to some extent in DMSO respiration, but not in nitrate respiration. In strain AN70 (ubiE) the lack of ubiquinone (Q) is due to a defect in a specific methylation step of Q biosynthesis. Synthesis of MK from DMK appears to depend on the same gene (ubiE).
已知缺乏泛醌的大肠杆菌突变株AN70(ubiE)(Young IG等人,1971年),对其甲萘醌(MK)和去甲基甲萘醌(DMK)含量进行了分析。与野生型相比,菌株AN70仅含有DMK,而没有MK。该突变株能够以富马酸、三甲胺N-氧化物(TMAO)和二甲基亚砜(DMSO)作为电子受体生长,但不能以硝酸盐作为电子受体生长。这些膜催化以富马酸和TMAO进行的厌氧呼吸,速率分别为野生型的69%和74%。DMSO呼吸降至野生型活性的38%,硝酸盐呼吸缺失(小于或等于野生型的8%),尽管野生型中相应的酶以正常速率存在。这些结果补充了早期的研究发现,即仅证明DMK在TMAO呼吸中起作用(Wissenbach等人,1990年)。得出的结论是,DMK(除MK外)可作为富马酸、TMAO以及在一定程度上DMSO呼吸中的氧化还原介质,但不能作为硝酸盐呼吸中的氧化还原介质。在菌株AN70(ubiE)中,泛醌(Q)的缺乏是由于Q生物合成中特定甲基化步骤的缺陷。从DMK合成MK似乎依赖于同一个基因(ubiE)。