Metabolism of cyclohexaneacetic acid and cyclohexanebutyric acid by Arthrobacter sp. strain CA1
Metabolism of cyclohexaneacetic acid and cyclohexanebutyric acid by Arthrobacter sp. strain CA1
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DOI：
10.1128/jb.150.3.1172-1182.1982
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发表时间：
1982-06
影响因子：
3.2
通讯作者：
H. Ougham;P. Trudgill
中科院分区：
文献类型：
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作者：
H. Ougham;P. Trudgill
以环己烷乙酸为唯一碳源，通过富集培养，分离到一株节杆菌，其生长倍增时间为4.2h。除了与环己烷乙酸盐一起生长外，该微生物还与浓度不超过0.05%的环己烷丁酸盐以及各种脂环酮和醇一起生长。环己烷乙酸酯的氧化通过辅酶A（CoA）酯的形成进行，随后引发β-氧化循环。在第二脱氢步骤之前，由于叔醇的形成，β-氧化被阻断，并且侧链通过（1-羟基环己-1-基）乙酰辅酶A裂解酶的作用作为乙酰辅酶A被消除。由此形成的环己酮通过充分描述的途径降解，该途径涉及通过生物Baeyer-Villiger加氧酶插入环氧。在无细胞提取物中证明了拟定代谢序列的所有酶。节杆菌属菌株CA 1合成了组成型β-氧化酶，但在与脂环酸一起生长的过程中，可能会进一步诱导对环己烷乙酸及其代谢产物具有活性的酶。其他酶的序列，（1-羟基环己烷-1-基）乙酰辅酶A裂解酶和酶的环己酮氧化，目前在琥珀酸盐生长的细胞，但诱导生长与环己烷乙酸在可忽略不计的水平。通过单一β-氧化循环将环己烷丁酸的氧化整合到环己烷乙酸氧化的途径中。该化合物的氧化可分为两个阶段。初始氧化为（1-羟基环己烷-1-基）乙酸酯可由组成酶催化，而（1-羟基环己烷-1-基）乙酸酯的进一步降解依赖于诱导的酶合成，其可被氯霉素抑制，从而积累环己烷乙酸酯和（1-羟基环己烷-1-基）乙酸酯。
A strain of Arthrobacter was isolated by enrichment culture with cyclohexaneacetate as the sole source of carbon and grew with a doubling time of 4.2 h. In addition to growing with cyclohexaneacetate, the organism also grew with cyclohexanebutyrate at concentrations not above 0.05%, and with a variety of alicyclic ketones and alcohols. Oxidation of cyclohexaneacetate proceeded through formation of the coenzyme A (CoA) ester followed by initiation of a beta-oxidation cycle. beta-Oxidation was blocked before the second dehydrogenation step due to the formation of a tertiary alcohol, and the side chain was eliminated as acetyl-CoA by the action of (1-hydroxycyclohexan-1-yl)acetyl-CoA lyase. The cyclohexanone thus formed was degraded by a well-described route that involves ring-oxygen insertion by a biological Baeyer-Villiger oxygenase. All enzymes of the proposed metabolic sequence were demonstrated in cell-free extracts. Arthrobacter sp. strain CA1 synthesized constitutive beta-oxidative enzymes, but further induction of enzymes active toward cyclohexaneacetate and its metabolites could occur during growth with the alicyclic acid. Other enzymes of the sequence, (1-hydroxycyclohexan-1-yl)acetyl-CoA lyase and enzymes of cyclohexanone oxidation, were present at negligible levels in succinate-grown cells but induced by growth with cyclohexaneacetate. The oxidation of cyclohexanebutyrate was integrated into the pathway for cyclohexaneacetate oxidation by a single beta-oxidation cycle. Oxidation of the compound could be divided into two phases. Initial oxidation to (1-hydroxycyclohexan-1-yl)acetate could be catalyzed by constitutive enzymes, whereas the further degradation of (1-hydroxycyclohexan-1-yl)acetate was dependent on induced enzyme synthesis which could be inhibited by chloramphenicol with the consequent accumulation of cyclohexaneacetate and (1-hydroxycyclohexan-1-yl)acetate.