Unden G
Institut für Mikrobiologie, J. W. Goethe-Universität, Frankfurt am Main, Federal Republic of Germany.
Arch Microbiol. 1988;150(5):499-503. doi: 10.1007/BF00422294.
Escherichia coli grown with glucose in the absence of added electron acceptors contained 3-4 times more naphthoquinones (menaquinone plus demethylmenaquinone) than in the presence of O2. Presence of electron acceptors resulted in a slight additional increase of the naphthoquinone content. A strain defective in the fnr gene, which encodes the transcriptional activator of anaerobic respiration, showed the same response. With fumarate or dimethyl sulfoxide present, 94% of the naphthoquinones consisted of menaquinone, while with nitrate up to 78% was demethylmenaquinone. With trimethylamine N-oxid as the acceptor the proportion was intermediate. From the donor substrates of anaerobic respiration only glycerol had a significant influence on the ratio of the contents of the 2 quinones. It is concluded that FNR, the gene product of the fnr gene, is not required for anaerobic derepression of naphthoquinone biosynthesis. Menaquinone appears to be involved specifically in the respiration with fumarate or dimethyl sulfoxide, and demethylmenaquinone in nitrate respiration. Both naphthoquinones appear to serve in trimethylamine N-oxide respiration.
在没有添加电子受体的情况下,以葡萄糖培养的大肠杆菌所含的萘醌(甲基萘醌加去甲基甲基萘醌)比在有氧条件下多3 - 4倍。电子受体的存在导致萘醌含量略有额外增加。编码厌氧呼吸转录激活因子的fnr基因缺陷型菌株表现出相同的反应。当存在富马酸盐或二甲基亚砜时,94%的萘醌由甲基萘醌组成,而当存在硝酸盐时,高达78%是去甲基甲基萘醌。以三甲胺N - 氧化物作为受体时,比例处于中间。在厌氧呼吸的供体底物中,只有甘油对这两种醌含量的比例有显著影响。得出的结论是,fnr基因的基因产物FNR对于萘醌生物合成的厌氧去阻遏不是必需的。甲基萘醌似乎特别参与与富马酸盐或二甲基亚砜的呼吸作用,而去甲基甲基萘醌参与硝酸盐呼吸作用。两种萘醌似乎都参与三甲胺N - 氧化物呼吸作用。