Ketner G, Campbell A
Proc Natl Acad Sci U S A. 1974 Jul;71(7):2698-702. doi: 10.1073/pnas.71.7.2698.
A deletion has been isolated which fuses galK and presumably galT to the promoter and operator of the bioA operon. The deletion has endpoints in bioA and galE, and leaves the operator-proximal end of bioA intact and the regulatory sites themselves functional. In bacterial strains which carry the deletion, the expression of galK is regulated by biotin, although due to the inefficiency of the bioA promoter even the fully derepressed level of galactokinase is low. Electron micrographic examination of the mutation shows that it is a simple deletion, uncomplicated by other chromosomal abnormalities.
已分离出一种缺失，它将galK（可能还有galT）与bioA操纵子的启动子和操纵基因融合。该缺失的端点位于bioA和galE中，使bioA靠近操纵基因的一端保持完整，且调控位点本身功能正常。在携带该缺失的细菌菌株中，galK的表达受生物素调控，尽管由于bioA启动子效率低下，即使半乳糖激酶完全去阻遏时的水平也很低。对该突变的电子显微镜检查表明，它是一个简单的缺失，未伴有其他染色体异常。
