Gibson J, Dispensa M, Harwood C S
Section of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, New York 14853, USA.
J Bacteriol. 1997 Feb;179(3):634-42. doi: 10.1128/jb.179.3.634-642.1997.
The anaerobic degradation of 4-hydroxybenzoate is initiated by the formation of 4-hydroxybenzoyl coenzyme A, with the next step proposed to be a dehydroxylation to benzoyl coenzyme A, the starting compound for a central pathway of aromatic compound ring reduction and cleavage. Three open reading frames, divergently transcribed from the 4-hydroxybenzoate coenzyme A ligase gene, hbaA, were identified and sequenced from the phototrophic bacterium Rhodopseudomonas palustris. These genes, named hbaBCD, specify polypeptides of 17.5, 82.6, and 34.5 kDa, respectively. The deduced amino acid sequences show considerable similarities to a group of hydroxylating enzymes involved in CO, xanthine, and nicotine metabolism that have conserved binding sites for [2Fe-2S] clusters and a molybdenum cofactor. Cassette disruption of the hbaB gene yielded a mutant that was unable to grow anaerobically on 4-hydroxybenzoate but grew normally on benzoate. The hbaB mutant cells did not accumulate [14C]benzoyl coenzyme A during short-term uptake of [14C]4-hydroxybenzoate, but benzoyl coenzyme A was the major radioactive metabolite formed by the wild type. In addition, crude extracts of the mutant failed to convert 4-hydroxybenzoyl coenzyme A to benzoyl coenzyme A. This evidence indicates that the hbaBCD genes encode the subunits of a 4-hydroxybenzoyl coenzyme A reductase (dehydroxylating). The sizes of the specified polypeptides are similar to those reported for 4-hydroxybenzoyl coenzyme A reductase isolated from the denitrifying bacterium Thauera aromatica. The amino acid consensus sequence for a molybdenum cofactor binding site is in HbaC. This cofactor appears to be an essential component because anaerobic growth of R. palustris on 4-hydroxybenzoate, but not on benzoate, was retarded unless 0.1 microM molybdate was added to the medium. Neither tungstate nor vanadate replaced molybdate, and tungstate competitively inhibited growth stimulation by molybdate.
4-羟基苯甲酸的厌氧降解始于4-羟基苯甲酰辅酶A的形成,下一步推测是脱羟基生成苯甲酰辅酶A,这是芳香族化合物环还原和裂解中心途径的起始化合物。从光合细菌沼泽红假单胞菌中鉴定并测序了三个与4-羟基苯甲酸辅酶A连接酶基因hbaA反向转录的开放阅读框。这些基因命名为hbaBCD,分别编码17.5、82.6和34.5 kDa的多肽。推导的氨基酸序列与参与一氧化碳、黄嘌呤和尼古丁代谢的一组羟化酶有相当大的相似性,这些酶具有保守的[2Fe-2S]簇和钼辅因子结合位点。hbaB基因的盒式破坏产生了一个突变体,该突变体不能在4-羟基苯甲酸上厌氧生长,但在苯甲酸上能正常生长。hbaB突变体细胞在短期摄取[14C]4-羟基苯甲酸过程中没有积累[14C]苯甲酰辅酶A,但苯甲酰辅酶A是野生型形成的主要放射性代谢物。此外,突变体的粗提物未能将4-羟基苯甲酰辅酶A转化为苯甲酰辅酶A。这一证据表明,hbaBCD基因编码4-羟基苯甲酰辅酶A还原酶(脱羟基)的亚基。指定多肽的大小与从反硝化细菌芳香索氏菌中分离的4-羟基苯甲酰辅酶A还原酶报道的大小相似。钼辅因子结合位点的氨基酸共有序列在HbaC中。该辅因子似乎是一个必需成分,因为除非向培养基中添加0.1 microM钼酸盐,沼泽红假单胞菌在4-羟基苯甲酸上的厌氧生长会受到抑制,但在苯甲酸上不会。钨酸盐和钒酸盐都不能替代钼酸盐,并且钨酸盐竞争性抑制钼酸盐对生长的刺激作用。