期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1974
卷号：71
期号：7
页码：2698-2702
DOI：10.1073/pnas.71.7.2698
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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.
