Andersen L, Kilstrup M, Neuhard J
University of Copenhagen, Institute of Biological Chemistry B, Denmark.
Arch Microbiol. 1989;152(2):115-8. doi: 10.1007/BF00456087.
Cytosine deaminase, encoded by the codA gene in Escherichia coli catalyzes the deamination of cytosine to uracil and ammonia. Regulation of codA expression was studied by determining the level of cytosine deaminase in E. coli K12 grown in various defined media. Addition of either pyrimidine or purine nucleobases to the growth medium caused repressed enzyme levels, whereas growth on a poor nitrogen source such as proline resulted in derepression of cytosine deaminase synthesis. Derepression of codA expression was induced by starvation for either uracil or cytosine nucleotides. Nitrogen control was found to be mediated by the glnLG gene products, and purine repression required a functional purR gene product. Studies with strains harbouring multiple mutations affecting both pyrimidine, purine and nitrogen control revealed that the overall regulation of cytosine deaminase synthesis by the different metabolites is cumulative.
胞嘧啶脱氨酶由大肠杆菌中的codA基因编码，催化胞嘧啶脱氨生成尿嘧啶和氨。通过测定在各种限定培养基中生长的大肠杆菌K12中胞嘧啶脱氨酶的水平，研究了codA表达的调控。向生长培养基中添加嘧啶或嘌呤核碱基会导致酶水平受到抑制，而在如脯氨酸这样的贫氮源上生长则会导致胞嘧啶脱氨酶合成的去抑制。尿嘧啶或胞嘧啶核苷酸饥饿会诱导codA表达的去抑制。发现氮调控由glnLG基因产物介导，嘌呤抑制需要功能性的purR基因产物。对携带影响嘧啶、嘌呤和氮调控的多种突变的菌株进行的研究表明，不同代谢物对胞嘧啶脱氨酶合成的总体调控是累积性的。
