Pascal M C, Burini J F, Ratouchniak J, Chippaux M
Mol Gen Genet. 1982;188(1):103-6. doi: 10.1007/BF00333001.
Introduction of chlA, B or E mutant alleles into strains carrying fusions between the lac structural genes and the promoter of the nitrate reductase operon led to the partial or total constitutive expression of the fusion. Presence of chlD mutated alleles in the same strains did not result in constitutive expression of the fusion and allowed full induction by nitrate only in the presence of molybdenum. It is proposed that the molybdenum cofactor, Mo-X, of the nitrate reductase is also corepressor of the operon. The chlA, B and E genes would be involved in the biosynthesis of the X-moity. Mutations in these genes would give an altered X-moity which still binds to molybdenum but leads to a less efficient repressor complex; chlD gene would code for an enzyme inserting molybdenum in the X-moity of the cofactor. Mutations in chlD give an empty cofactor leading to a complex which permanently represses the operon unless molybdenum is added.
将chlA、B或E突变等位基因导入携带乳糖结构基因与硝酸还原酶操纵子启动子融合体的菌株中，会导致融合体部分或完全组成型表达。在相同菌株中存在chlD突变等位基因不会导致融合体组成型表达，并且仅在有钼存在时才允许硝酸盐完全诱导。有人提出，硝酸还原酶的钼辅因子Mo-X也是该操纵子的共阻遏物。chlA、B和E基因可能参与X部分的生物合成。这些基因中的突变会产生改变的X部分，其仍能与钼结合，但会导致阻遏复合物效率降低；chlD基因编码一种将钼插入辅因子X部分的酶。chlD中的突变会产生一个空的辅因子，导致一个复合物永久抑制操纵子，除非添加钼。
